inositol-1-4-5-trisphosphate and Pneumonia--Viral

Estrogen hormone acts as a potential key player in providing immunity against certain viral infection. It is found to be associated in providing immunity against acute lungs inflammation and influenza virus by modulating cytokines storm and mediating adaptive immune alterations respectively. Women are less affected by SARS-CoV-2 infection because of the possible influence of estrogen hormone as compared to men. We hypothesized that SARS-CoV-2 causes stress in endoplasmic reticulum (ER) which in turn aggravates the infection, estrogen hormone might play key role in decreasing ER stress by activating estrogen mediated signaling pathways, results in unfolded protein response (UPR). Estrogen governs degradation of phosphotidylinositol 4,5-bisphosphate (PIP

Topics: Adult; Betacoronavirus; Coronavirus Infections; COVID-19; Datasets as Topic; Diglycerides; Disease Resistance; Endoplasmic Reticulum Stress; Estrogens; Female; Humans; Inositol 1,4,5-Trisphosphate; Male; Middle Aged; Models, Biological; Pakistan; Pandemics; Phosphatidylinositol 4,5-Diphosphate; Pneumonia, Viral; SARS-CoV-2; Sex Characteristics; Sex Distribution; Signal Transduction; Type C Phospholipases; Unfolded Protein Response; Viral Proteins

Tobacco smoking may predispose humans to respiratory disease, and may be a compounding risk factor in HIV infection and progression to AIDS. We have demonstrated that chronic exposure of mice and rats to cigarette smoke or nicotine inhibits T cell responsiveness, which may account for the decreased antibody response to T-dependent antigens seen in these animals. This inhibition may result from aberrant antigen-mediated signaling and depletion of IP3-sensitive Ca2+ stores in nicotine-treated animals. Moreover, nicotine appears to moderate the inflammation associated with turpentine-induced sterile abscess and influenza infection. These anti-inflammatory properties of nicotine may account for longer survival of nicotine-treated than control mice lethally infected with influenza virus. However, because inflammation is required for clearance of many pathogens, nicotine-treated mice exhibit significantly higher titers of influenza virus following infection. These results offer an explanation for the higher susceptibility to some infectious diseases, but greater resistance to some inflammatory diseases among human smokers.

Topics: Abscess; Animals; Calcium; Fever; Immunosuppressive Agents; Influenza A virus; Inositol 1,4,5-Trisphosphate; Mice; Nicotine; Orthomyxoviridae Infections; Pneumonia, Viral; Rats; Rats, Inbred Lew; Receptors, Antigen, T-Cell; T-Lymphocytes; Turpentine