ovalbumin and Rodent-Diseases

Infections with pinworms are common in rodent animal facilities. In this study, we show the consequence of an outbreak in a transgenic barrier facility of infection by Syphacia obvelata, a murine pinworm gastrointestinal nematode. Immune responses were defined in experimental infection studies with BALB/c mice. Infection with S. obvelata induced a transient Th2-type immune response with elevated interleukin 4 (IL-4), IL-5, and IL-13 cytokine production and parasite-specific immunoglobulin G1 (IgG1). In contrast, BALB/c mice deficient in IL-13, IL-4/13, or the IL-4 receptor alpha chain showed chronic disease, with a >100-fold higher parasite burden, increased gamma interferon production, parasite-specific IgG2b, and a default Th2 response. Interestingly, infected IL-4-/- BALB/c mice showed only slightly elevated parasite burdens compared to the control mice, suggesting that IL-13 plays the dominant role in the control of S. obvelata. The influence that pinworm infection has on the allergic response to a dietary antigen was found to be important. Helminth-infected mice immunized against ovalbumin (Ova) elicited more severe anaphylactic shock with reduced Ova-specific IL-4 and IL-5 than did noninfected controls, demonstrating that S. obvelata infection is able to influence nonrelated laboratory experiments. The latter outcome highlights the importance of maintaining mice for use as experimental models under pinworm-free conditions.

Topics: Animals; Chemokines; Enterobiasis; Enterobius; Hypersensitivity; Immunoglobulin G; Interleukins; Mice; Mice, Inbred BALB C; Mice, Mutant Strains; Ovalbumin; Receptors, Cell Surface; Rodent Diseases; Th2 Cells

The effects of interferon (IFN)-gamma induced by virus infection on eosinophil reaction in allergic airway inflammation are not yet clear. We investigated the effects of lactic dehydrogenase virus (LDV) infection, which increases IFN -gamma production with no viral infection or replication in respiratory epithelium, on allergic airway hypersensitivity. LDV infection suppressed antigen-induced eosinophil recruitment into the airway in sensitized mice. IL -5 gene expression in bronchoalveolar lavage (BAL) cells was significantly suppressed in LDV -infected mice compared with uninfected controls. The numbers of total T cells and CD 4+ T cells were significantly reduced in LDV -infected mice compared with controls. The present results suggested that the increase in production of IFN -gamma by viral infection suppresses the eosinophil reaction, and this suppressive effect may be mediated by inhibition of the recruitment of CD 4+ T cell and IL -5 production.

Topics: Allergens; Animals; Arterivirus Infections; Base Sequence; Bronchoalveolar Lavage; CD4-Positive T-Lymphocytes; Eosinophils; Gene Expression Regulation; Hypersensitivity; Interferon-gamma; Interleukin-5; Lactate dehydrogenase-elevating virus; Male; Mice; Ovalbumin; Respiratory System; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Rodent Diseases

Two groups of pregnant guinea pigs were sensitized to ovalbumin (OA) by injecting the antigen, incorporated in Freund's incomplete or complete adjuvant, via the IM or foot pad route, respectively. Inoculation of OA into the lumen of the mammary glands during subsequent lactation elicited an influx of leukocytes into the milk only in guinea pigs exhibiting OA-specific delayed-type cutaneous hypersensitivity (DTCH); ie, only in the animals that previously were given OA in Freund's complete adjuvant. Lactating female guinea pigs, passively sensitized to OA by immune serum obtained from donors that exhibited specific DTCH, did not respond top intramammary inoculation of OA. Recipients of peritoneal exudate cells, obtained from syngeneic donors that exhibited DTCH to OA, in turn exhibited DTCH and responded to intramammary inoculation of OA with a transient release of leukocytes into the milk. Emigration of leukocytes into the milk, elicited by antigen in specifically sensitized hosts, appeared to be a local expression of a general state of lymphocyte-dependent hypersensitivity.

Topics: Animals; Dermatitis, Atopic; Disease Models, Animal; Female; Freund's Adjuvant; Guinea Pigs; Immunity, Cellular; Lactation; Mammary Glands, Animal; Milk; Ovalbumin; Pregnancy; Rodent Diseases

Topics: Aluminum Hydroxide; Analysis of Variance; Anaphylaxis; Animals; Antibody Specificity; Asthma; Bordetella pertussis; Bronchial Spasm; Disease Models, Animal; Dose-Response Relationship, Drug; Female; Immunization; Immunoglobulin E; Immunoglobulin G; Lung; Ovalbumin; Passive Cutaneous Anaphylaxis; Pressure; Rats; Rodent Diseases; Time Factors