interleukin-8 and Orthomyxoviridae-Infections

The expanding knowledge on the systemic influence of the human microbiome suggests that fecal samples are underexploited sources of new beneficial strains for extra-intestinal health. We have recently shown that acetate, a main circulating microbiota-derived molecule, reduces the deleterious effects of pulmonary

Topics: Animals; Clostridiales; Disease Models, Animal; Humans; Influenza, Human; Interleukin-8; Mice; Orthomyxoviridae Infections; Pneumococcal Infections; Salmonella Infections, Animal; Salmonella typhimurium; Streptococcus pneumoniae

Based on Janus kinase 1/2-signal transducer and activator of transcription 1(JAK1/2-STAT1) signaling pathway, this study explored the immune mechanism of Maxing Shigan Decoction in alleviating the lung tissue and colon tissue damage in mice infected with influenza virus. The influenza virus infection was induced in mice by nasal drip of influenza virus. The normal group, model group, oseltamivir group, antiviral granule group, and Maxing Shigan Decoction group were designed. After intragastric administration of corresponding drugs or normal saline for 3 or 7 days, the body mass was measured, and lung index, spleen index, and thymus index were calculated. Based on hematoxylin-eosin(HE) staining, the pathological changes of lung tissue and colon tissue were observed. Enzyme-linked immunosorbent assay(ELISA) was used to detect serum levels of inflammatory factors interleukin-8(IL-8) and interferon-γ(IFN-γ), Western blot and real-time quantitative polymerase chain reaction(RT-qPCR) to determine the protein and mRNA levels of JAK1, JAK2, STAT1, interferon regulatory factor 9(IRF9), and IFN-γ in lung tissue and colon tissue. The results showed that after 3 and 7 days of administration, the body mass, spleen index, and thymus index were lower(P<0.05 or P<0.01), and the lung index was higher(P<0.01) in the model group than in the normal group. Moreover, the model group showed congestion, edema, and infiltration of a large number of lymphocytes and macrophages in the lung tissue, irregular structure of colon mucosa, ulceration and shedding of epithelial cells, and infiltration of a large number of inflammatory cells. The model group had higher levels of serum IFN-γ(P<0.01), higher protein and mRNA expression of JAK1, JAK2, STAT1, IRF9, IFN-γ in lung tissue(P<0.05 or P<0.01), higher level of JAK2 protein in colon tissue(P<0.01), and higher protein and mRNA levels of STAT1 and IRF9(P<0.05 or P<0.01) than the normal group. Compared with the model group, Maxing Shigan Decoction group had high body mass, spleen index, and thymus index(P<0.05 or P<0.01), low lung index(P<0.05 or P<0.01), and significant alleviation of pathological injury in lung and colon. Moreover, lower serum level of IFN-γ(P<0.05 or P<0.01), protein and mRNA levels of JAK1, JAK2, STAT1, IRF9, and IFN-γ in lung tissue(P<0.05 or P<0.01), JAK2 protein level in colon tissue(P<0.01), and protein and mRNA levels of STAT1 and IRF9(P<0.05 or P<0.01)

Topics: Animals; Colon; Humans; Influenza, Human; Interferon-gamma; Interleukin-8; Janus Kinase 1; Lung; Mice; Orthomyxoviridae; Orthomyxoviridae Infections; RNA, Messenger; Signal Transduction; STAT1 Transcription Factor

The Madin-Darby canine kidney (MDCK) cell line is typically used to analyze pathological features after canine influenza virus (CIV) infection. However, MDCK cells are not the ideal cell type, because they are kidney epithelial cells. Therefore, we generated an immortalized canine tracheal epithelial cell line, KU-CBE, to more reliably study immune responses to CIV infection in the respiratory tract. KU-CBE cells expressed the influenza virus receptor, α-2,3-sialic acid (SA), but not α-2,6-SA. KU-CBE and MDCK cells infected with H3N2 CIV demonstrated comparable virus growth kinetics. Gene expression levels of interleukin (IL)-1β, IL-2, IL-4, IL-6, IL-8, IL-10, tumor necrosis factor (TNF)-α, and interferon (IFN)-β were estimated in both KU-CBE and MDCK cells infected with CIV by real-time reverse transcription polymerase chain reaction (qRT-PCR). Of these cytokines, IL-4, IL-10, TNF-α, and IFN-β mRNAs were detected in both cell lines. Gene expression of IL-4, IL-10, and TNF-α was not significantly different in the two cell lines. However, MDCK cells exhibited a significantly higher level of IFN-β mRNA than KU-CBE cells at 18 h post infection. Additionally, the protein concentrations of these four cytokines were determined by enzyme-linked immunosorbent assay (ELISA) using cell culture supernatants obtained from the two CIV-infected cell lines. MDCK cells produced significantly higher amounts of IL-4 and IFN-β than KU-CBE cells. However, KU-CBE cells produced a significantly higher amount of TNF-α than MDCK cells. These data indicated that the newly developed canine tracheal epithelial cells exhibited different cytokine production patterns compared to MDCK cells when infected with CIV. Inflammation of the respiratory tract of dogs induced by CIV infection may be attributed to the elevated expression level of TNF-α in canine tracheal epithelial cells.

Topics: Animals; Cell Line; Cytokines; Dog Diseases; Dogs; Influenza A Virus, H3N2 Subtype; Interferon-beta; Interleukin-10; Interleukin-1beta; Interleukin-2; Interleukin-4; Interleukin-6; Interleukin-8; Madin Darby Canine Kidney Cells; Orthomyxoviridae Infections; Real-Time Polymerase Chain Reaction; Respiratory Mucosa; Trachea; Tumor Necrosis Factor-alpha

Orf virus (ORFV), a member of parapoxvirus, is an enveloped virus with genome of double-stranded DNA. ORFV causes contagious pustular dermatitis or contagious ecthyma in sheep and goats worldwide. In general, detection of viral DNA and observing ORFV virion in tissues of afflicted animals are two methods commonly used for diagnosis of orf infection; however, isolation of the ORFV in cell culture using virus-containing tissue as inoculum is known to be difficult. In this work, the ORFV (Hoping strain) isolated in central Taiwan was successfully grown in cell culture. We further examined the biochemical characteristic of our isolate, including viral genotyping, viral mRNA and protein expression. By electron microscopy, one unique form of viral particle from ORFV infected cellular lysate was demonstrated in the negative-stained field. Moreover, immunomodulating and anti-influenza virus properties of this ORFV were investigated. ORFV stimulated human monocytes (THP-1) secreting proinflammatory cytokines IL-8 and TNF-α. And, pre-treatment of ORFV-infected cell medium prevents A549 cells from subsequent type A influenza virus (IAV) infection. Similarly, mice infected with ORFV via both intramuscular and subcutaneous routes at two days prior to IAV infection significantly decreased the replication of IAV. In summary, the results of a current study indicated our Hoping strain harbors the immune modulator property; with such a bio-adjuvanticity, we further proved that pre-exposure of ORFV protects animals from subsequent IAV infection.

Topics: Animals; Cells, Cultured; Coinfection; DNA, Viral; Ecthyma, Contagious; Female; Goat Diseases; Goats; Humans; Influenza A virus; Influenza, Human; Interleukin-8; Mice; Mice, Inbred BALB C; Monocytes; Orf virus; Orthomyxoviridae Infections; Polymerase Chain Reaction; Taiwan; Tumor Necrosis Factor-alpha

Infection of the lower respiratory tract by influenza A viruses results in increases in inflammation and immune cell infiltration in the lung. The dynamic relationships among the lung microenvironments, the lung, and systemic host responses during infection remain poorly understood. Here we used extensive systematic histological analysis coupled with live imaging to gain access to these relationships in ferrets infected with the 2009 H1N1 pandemic influenza A virus (H1N1pdm virus). Neutrophil levels rose in the lungs of H1N1pdm virus-infected ferrets 6 h postinfection and became concentrated at areas of the H1N1pdm virus-infected bronchiolar epithelium by 1 day postinfection (dpi). In addition, neutrophil levels were increased throughout the alveolar spaces during the first 3 dpi and returned to baseline by 6 dpi. Histochemical staining revealed that neutrophil infiltration in the lungs occurred in two waves, at 1 and 3 dpi, and gene expression within microenvironments suggested two types of neutrophils. Specifically, CCL3 levels, but not CXCL8/interleukin 8 (IL-8) levels, were higher within discrete lung microenvironments and coincided with increased infiltration of neutrophils into the lung. We used live imaging of ferrets to monitor host responses within the lung over time with [(18)F]fluorodeoxyglucose (FDG). Sites in the H1N1pdm virus-infected ferret lung with high FDG uptake had high levels of proliferative epithelium. In summary, neutrophils invaded the H1N1pdm virus-infected ferret lung globally and focally at sites of infection. Increased neutrophil levels in microenvironments did not correlate with increased FDG uptake; hence, FDG uptake may reflect prior infection and inflammation of lungs that have experienced damage, as evidenced by bronchial regeneration of tissues in the lungs at sites with high FDG levels.. Severe influenza disease is characterized by an acute infection of the lower airways that may progress rapidly to organ failure and death. Well-developed animal models that mimic human disease are essential to understanding the complex relationships of the microenvironment, organ, and system in controlling virus replication, inflammation, and disease progression. Employing the ferret model of H1N1pdm virus infection, we used live imaging and comprehensive histological analyses to address specific hypotheses regarding spatial and temporal relationships that occur during the progression of infection and inflammation. We show the general invasion of neutrophils at the organ level (lung) but also a distinct pattern of localized accumulation within the microenvironment at the site of infection. Moreover, we show that these responses were biphasic within the lung. Finally, live imaging revealed an early and sustained host metabolic response at sites of infection that may reflect damage and repair of tissues in the lungs.

Topics: Animals; Chemokine CCL2; Chemokine CCL3; Female; Ferrets; Fluorodeoxyglucose F18; Gene Expression; Influenza A Virus, H1N1 Subtype; Interleukin-8; Lung; Neutrophil Infiltration; Neutrophils; Orthomyxoviridae Infections; Positron-Emission Tomography; Respiratory Tract Infections

We studied the pathogenesis and transmissibility of a novel avian-origin H7N9 influenza virus in pigs. When pigs were infected with H7N9 influenza virus, they did not show any clear clinical signs (such as sneezing, fever and loss of body weight), and they shed viruses through their noses for 2 days after infection. No transmission occurred between infected and naïve pigs. Pigs suffered from mild pneumonia, which was accompanied by the induction of inflammatory cytokines and chemokines such as IL-8 and CCL1. Taken together, our results suggest that pigs may not play an active role in transmitting H7N9 influenza virus to mammals.

Topics: Animals; Chemokine CCL1; Disease Models, Animal; Influenza A Virus, H7N9 Subtype; Interleukin-8; Lung; Orthomyxoviridae Infections; Pneumonia; RNA, Viral; Swine; Viral Load; Virus Shedding

Influenza A virus causes a highly contagious respiratory disease in a variety of avian and mammalian hosts, including humans and pigs. The primary means for preventing influenza epidemics is vaccination. Epitope-based vaccine represents a new approach to achieve protective immunity. The objective of this study was to construct and evaluate the immunogenicity of an epitope-based antigen for its potential application in future influenza vaccine development. The antigen, comprised of a set of consensus influenza A virus epitopes (IAVe), was genetically linked to a subunit of the bacterial heat-labile enterotoxin (LTB) as an adjuvant. Immunogenicity of this LTB-IAVe antigen was evaluated in a pig model. Despite an inability to detect neutralizing antibodies directed toward the whole virus, humoral immunity against the IAVe was demonstrated in both serum (IgA and IgG) and mucosal secretions (IgG) of immunized pigs. Specific cellular immunity was also induced after LTB-IAVe immunization, as evidenced by up-regulating of IL-1β, IL-8, and IL-4 expression in peripheral blood mononuclear cells (PBMCs) of vaccinated pigs. In comparison to the non-immunized pigs, pigs immunized with the LTB-IAVe showed improved protection against a pathogenic H1N1 swine influenza virus challenge, with about 50% decrease of pneumonic lesions and 10-fold reduction of the viral load in lung and nasal secretion at five days post challenge. This study establishes a platform for future construction of epitope-based vaccines against influenza A virus infection.

Topics: Adjuvants, Immunologic; Animals; Antibodies, Neutralizing; Bacterial Toxins; Enterotoxins; Epitopes; Escherichia coli Proteins; Humans; Immunization; Immunogenetic Phenomena; Immunoglobulin A; Influenza A Virus, H1N1 Subtype; Influenza Vaccines; Interleukin-4; Interleukin-8; Leukocytes, Mononuclear; Orthomyxoviridae Infections; Swine; Swine Diseases

Influenza A virus (IAV) predisposes individuals to secondary infections with the bacterium Streptococcus pneumoniae (the pneumococcus). Infections may manifest as pneumonia, sepsis, meningitis, or otitis media (OM). It remains controversial as to whether secondary pneumococcal disease is due to the induction of an aberrant immune response or IAV-induced immunosuppression. Moreover, as the majority of studies have been performed in the context of pneumococcal pneumonia, it remains unclear how far these findings can be extrapolated to other pneumococcal disease phenotypes such as OM. Here, we used an infant mouse model, human middle ear epithelial cells, and a series of reverse-engineered influenza viruses to investigate how IAV promotes bacterial OM. Our data suggest that the influenza virus HA facilitates disease by inducing a proinflammatory response in the middle ear cavity in a replication-dependent manner. Importantly, our findings suggest that it is the inflammatory response to IAV infection that mediates pneumococcal replication. This study thus provides the first evidence that inflammation drives pneumococcal replication in the middle ear cavity, which may have important implications for the treatment of pneumococcal OM.

Topics: Animals; Inflammation; Influenza A virus; Interleukin-6; Interleukin-8; Mice; Mice, Inbred C57BL; Orthomyxoviridae Infections; Otitis Media; Pneumococcal Infections; Viral Load

Influenza A virus (IAV) is a worldwide public health problem causing 500,000 deaths each year. Palmitoyl-oleoyl-phosphatidylglycerol (POPG) is a minor component of pulmonary surfactant, which has recently been reported to exert potent regulatory functions upon the innate immune system. In this article, we demonstrate that POPG acts as a strong antiviral agent against IAV. POPG markedly attenuated IL-8 production and cell death induced by IAV in cultured human bronchial epithelial cells. The lipid also suppressed viral attachment to the plasma membrane and subsequent replication in Madin-Darby canine kidney cells. Two virus strains, H1N1-PR8-IAV and H3N2-IAV, bind to POPG with high affinity, but exhibit only low-affinity interactions with the structurally related lipid, palmitoyl-oleoyl-phosphatidylcholine. Intranasal inoculation of H1N1-PR8-IAV in mice, in the presence of POPG, markedly suppressed the development of inflammatory cell infiltrates, the induction of IFN-γ recovered in bronchoalveolar lavage, and viral titers recovered from the lungs after 5 days of infection. These findings identify supplementary POPG as a potentially important new approach for treatment of IAV infections.

Topics: Administration, Intranasal; Animals; Antiviral Agents; Bronchi; Cell Death; Cells, Cultured; Cytokines; Epithelial Cells; Female; Humans; Influenza A virus; Influenza A Virus, H1N1 Subtype; Influenza A Virus, H3N2 Subtype; Influenza, Human; Interleukin-8; Mice; Mice, Inbred BALB C; Orthomyxoviridae Infections; Phosphatidylglycerols; Phospholipids; Viral Proteins; Virus Replication

The triple reassortant H2N3 virus isolated from diseased pigs in the United States in 2006 is pathogenic for certain mammals without prior adaptation and transmits among swine and ferrets. Adaptation, in the H2 hemagglutinin derived from an avian virus, includes the ability to bind to the mammalian receptor, a significant prerequisite for infection of mammals, in particular humans, which poses a big concern for public health. Here we investigated the pathogenic potential of swine H2N3 in Cynomolgus macaques, a surrogate model for human influenza infection. In contrast to human H2N2 virus, which served as a control and largely caused mild pneumonia similar to seasonal influenza A viruses, the swine H2N3 virus was more pathogenic causing severe pneumonia in nonhuman primates. Both viruses replicated in the entire respiratory tract, but only swine H2N3 could be isolated from lung tissue on day 6 post infection. All animals cleared the infection whereas swine H2N3 infected macaques still presented with pathologic changes indicative of chronic pneumonia at day 14 post infection. Swine H2N3 virus was also detected to significantly higher titers in nasal and oral swabs indicating the potential for animal-to-animal transmission. Plasma levels of IL-6, IL-8, MCP-1 and IFNγ were significantly increased in swine H2N3 compared to human H2N2 infected animals supporting the previously published notion of increased IL-6 levels being a potential marker for severe influenza infections. In conclusion, the swine H2N3 virus represents a threat to humans with the potential for causing a larger outbreak in a non-immune or partially immune population. Furthermore, surveillance efforts in farmed pig populations need to become an integral part of any epidemic and pandemic influenza preparedness.

Topics: Animals; Chemokine CCL2; Female; Humans; Influenza A virus; Influenza A Virus, H2N2 Subtype; Interferon-gamma; Interleukin-6; Interleukin-8; Lung; Macaca fascicularis; Male; Orthomyxoviridae Infections; Pneumonia, Viral; Reassortant Viruses; Severity of Illness Index; Swine; Swine Diseases

The PB1-F2 protein of the influenza A viruses (IAVs) can act as a virulence factor in mice. Its contribution to the virulence of IAV in swine, however, remains largely unexplored. In this study, we chose two genetically related H3N2 triple-reassortant IAVs to assess the impact of PB1-F2 in virus replication and virulence in pigs. Using reverse genetics, we disrupted the PB1-F2 ORF of A/swine/Wisconsin/14094/99 (H3N2) (Sw/99) and A/turkey/Ohio/313053/04 (H3N2) (Ty/04). Removing the PB1-F2 ORF led to increased expression of PB1-N40 in a strain-dependent manner. Ablation of the PB1-F2 ORF (or incorporation of the N66S mutation in the PB1-F2 ORF, Sw/99 N66S) affected the replication in porcine alveolar macrophages of only the Sw/99 KO (PB1-F2 knockout) and Sw/99 N66S variants. The Ty/04 KO strain showed decreased virus replication in swine respiratory explants, whereas no such effect was observed in Sw/99 KO, compared with the wild-type (WT) counterparts. In pigs, PB1-F2 did not affect virus shedding or viral load in the lungs for any of these strains. Upon necropsy, PB1-F2 had no effect on the lung pathology caused by Sw/99 variants. Interestingly, the Ty/04 KO-infected pigs showed significantly increased lung pathology at 3 days post-infection compared with pigs infected with the Ty/04 WT strain. In addition, the pulmonary levels of interleukin (IL)-6, IL-8 and gamma interferon were regulated differentially by the expression of PB1-F2. Taken together, these results indicate that PB1-F2 modulates virus replication, virulence and innate immune responses in pigs in a strain-dependent fashion.

Topics: Animals; Cell Death; Cell Line; Dogs; HEK293 Cells; Humans; Immunity, Innate; Influenza A Virus, H3N2 Subtype; Interferon-gamma; Interleukin-6; Interleukin-8; Lung; Macrophages, Alveolar; Mutagenesis; Orthomyxoviridae Infections; Swine; Viral Load; Viral Proteins; Virulence; Virulence Factors; Virus Replication; Virus Shedding

Avian-lineage H3N2 canine influenza virus (CIV)-associated respiratory disease, which can be fatal, emerged in South Korean dogs in 2007. We show here that dogs experimentally infected with CIV only developed respiratory tract diseases, as no extrapulmonary lesions and virus antigens were detected. This differs from the multiorgan diseases that avian influenza H5N1 induces in small experimental animals. However, the CIV-infected dogs developed a distinctively severe, long-persistent bronchointerstitial pneumonia, which differs from the acute but short-term bronchopneumonia that human (H1N1 and H3N2) influenza cause in rodents and ferrets. Histopathology and in situ TUNEL assays revealed that the neutrophils infiltrating the lesions were undergoing apoptosis, which probably reflects the attempts by the body to maintain appropriate numbers of neutrophils for defense against secondary bacterial infections. Our observations suggest that neutrophils along with the related chemoattractant cytokines (TNF-alpha, IL-1 and IL-8, etc.) may play a key role in the pathogenesis of H3N2 CIV in dogs.

Topics: Animals; Apoptosis; Dog Diseases; Dogs; Humans; Influenza A Virus, H1N1 Subtype; Influenza A Virus, H3N2 Subtype; Influenza A Virus, H5N1 Subtype; Influenza, Human; Interleukin-1; Interleukin-8; Lung; Neutrophils; Orthomyxoviridae Infections; Trachea; Tumor Necrosis Factor-alpha

Influenza virus (Flu) infection and secondary complications are a leading cause of morbidity and mortality worldwide. The increasing number of annual Flu cases, coupled with the recent Flu pandemic, has amplified concerns about the impact of Flu on human and animal health. Similar to humans, Flu is problematic in pigs, not only as a primary pathogen but as an agent in polymicrobial pneumonia. Bordetella species play a role in mixed infections and often colonize the respiratory tract without overt clinical signs. Pigs serve as a valuable animal model for several respiratory pathogens, including Bordetella (Bb) and Flu. To investigate Flu/Bb coinfection pathogenesis, a study was completed in which pigs were inoculated with Flu-only, Bb-only or both agents (Flu/Bb). Results indicate that Flu clearance is not altered by Bb infection, but Flu does enhance Bb colonization. Pulmonary lesions in the Flu/Bb group were more severe when compared to Flu-only or Bb-only groups and Bb did not cause significant lesions unless pigs were coinfected with Flu. The type I interferon response was elevated in coinfected pigs, but increased expression of antiviral genes Mx and PKR did not appear to enhance Flu clearance in coinfected pigs, as viral clearance was similar between Flu/Bb and Flu-only groups. IL-1beta and IL-8 were elevated in lungs of coinfected pigs, correlating to the days enhanced lesions were observed. Overall, Flu infection increased Bb colonization and enhanced production of proinflammatory mediators that likely contribute to exacerbated pulmonary lesions.

Topics: Animals; Bordetella bronchiseptica; Bordetella Infections; Disease Models, Animal; eIF-2 Kinase; Female; GTP-Binding Proteins; Interferon Type I; Interleukin-1beta; Interleukin-8; Lung; Myxovirus Resistance Proteins; Orthomyxoviridae; Orthomyxoviridae Infections; Swine; Swine Diseases

Even though ferrets are one of the principal animal models for influenza pathogenesis, the lack of suitable immunological reagents has so far limited their use in host response studies. Using recently established real-time PCR assays for a panel of ferret cytokines, we analyzed the local ferret immune response to human influenza isolates of the H1N1 and H3N2 subtypes that varied in their virulence. We observed that the severity of clinical signs correlated with gross- and histopathological changes in the lungs and was subtype-independent. Strains causing a mild disease were associated with a strong and rapid innate response and upregulation of IL-8, while severe infections were characterized by a lesser induction of type I and II interferons and strong IL-6 upregulation. These findings suggest that more virulent strains may interfere more efficiently with the host response at early disease stages.

Topics: Animals; Body Temperature; Body Weight; Ferrets; Gene Expression Profiling; Influenza A Virus, H1N1 Subtype; Influenza A Virus, H3N2 Subtype; Interferons; Interleukin-6; Interleukin-8; Lung; Male; Molecular Sequence Data; Orthomyxoviridae Infections; Seasons; Severity of Illness Index

We investigated the effect of ferulic acid (FA) and isoferulic acid (IFA), which are active components of the rhizoma of Cimicifuga species used frequently as anti-inflammatory drugs in Japanese Oriental medicines, on murine interleukin-8 (IL-8) production in response to influenza virus infections in vitro and in vivo by antibody-sandwich enzyme-linked immunosorbent assay. In the in vitro study, the murine macrophage cell line RAW 264.7 was infected with influenza virus at a dose of 10 plaque forming units (PFU)/cell and cultured in the presence or absence of drugs. Both FA and IFA reduced the IL-8 levels in the 20-h conditioned medium in comparison with control in a dose-dependent manner. The effect of IFA was greater than that of FA: IL-8 levels were reduced to 43% and 56% of the control in the presence of 100 micrograms/ml of IFA and FA, respectively. In the in vivo study, mice were infected with 1,000 PFU of virus and received daily oral administrations of Cimicifuga heracleifolia extract (5 mg/mouse/day), FA (0.5 mg/mouse/day), IFA (0.125 mg/mouse/day), or phosphate buffered saline. The three drugs showed a tendency to reduce IL-8 levels in bronchoalveolar lavage (BAL) obtained 2 days after infection. Moreover, both FA and IFA also significantly reduced the number of exuded neutrophils into BAL. However, the drug administrations did not affect the virus yields in BAL. These data suggest that FA and IFA are novel and potent inhibitors of murine IL-8 production and might act as one of the main components of anti-inflammatory rhizoma of Cimicifuga species.

Topics: Animals; Antihypertensive Agents; Cell Line; Chick Embryo; Cinnamates; Coumaric Acids; Female; Influenza A virus; Interleukin-8; Lipopolysaccharides; Lung; Macrophages; Mice; Mice, Inbred ICR; Neutrophils; Orthomyxoviridae Infections; Plants, Medicinal

We investigated the interleukin-8 (IL-8)-producing activity of influenza A NWS virus in cultured rat kidney NRK-52E cells and a rat influenza model. The production of rat IL-8 increased significantly in the virus-infected cells but not in UV-inactivated virus- or split-product-treated cells. The increase in IL-8 production could be detected in the bronchoalveolar lavage of infected rats. These data suggest that infectious virus has the potential to accelerate the production of IL-8 in cultured cells and in vivo in airway-lining cells.

Topics: Animals; Bronchoalveolar Lavage Fluid; Cell Line; In Vitro Techniques; Influenza A virus; Interleukin-8; Male; Orthomyxoviridae Infections; Rats; Rats, Wistar; Time Factors