PubMed · 6120508
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D Davies. 1981. Bronchodilators.. https://pubmed.ncbi.nlm.nih.gov/6120508/
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To determine the role of humoral mucosal immune response in protection against shigellosis, we have obtained a monoclonal dimeric immunoglobulin A (IgA) antibody specific for Shigella flexneri serotype 5a lipopolysaccharide (mIgA) and used a murine pulmonary infection model that mimics the lesions occurring in natural intestinal infection. Adult BALB/c mice challenged with 10(7) S. flexneri organisms developed a rapid inflammatory response characterized by polymorphonuclear cell infiltration around and within the bronchi and strong systemic interleukin 6 response. Implantation of hybridoma cells in the back of mice, resulting in the development of a myeloma tumor producing mIgA in the serum and subsequently secretory mIgA in local secretions, or direct intranasal administration of these antibodies, protected the animals against subsequent intranasal challenge with S. flexneri serotype 5a. Absence of histopathological lesion and significant decrease in bacterial load of the lungs and of systemic interleukin 6 response were the three major criteria of protection. This protection was shown to be serotype-specific and dependent on local concentration of mIgA. These data demonstrate that mucosal antibodies directed against a single polysaccharidic surface epitope of Shigella can protect against the disease.
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The effect of murine rIL-4 on the development of herpesvirus encephalitis (HSE) in mice infected intranasally with herpes simplex virus type 1 (HSV-1) was investigated. The mortality rates of mice infected with a 0.5 LD50 dose of HSV-1 were greatly increased after the administration of rIL-4 at doses ranging from 0.01 to 1.0 U/mouse 2 h before and 2, 4 and 6 days after the infection. In contrast, survival rates of mice exposed to a 5 LD50 dose of HSV-1 were clearly increased when these mice were treated with anti-IL-4 mAb. Cervical lymph node (CLN) cells and cerebrospinal fluid (CSF) cells from mice with HSE (HSE mice) produced IL-4 in their culture fluids when they were stimulated in vitro with HSV-1 Ag. Increased amounts of HSV-1 infection in mice resulted in the increased production of IL-4 in the culture fluids of local lymphocytes. However, significant amounts of IL-4 were not produced in serum specimens or in culture fluids of spleen cells from HSE mice. IL-4 production in culture fluids of CLN and CSF cells from HSE mice was clearly reduced after treatment of HSE mice with anti-IL-4 mAb. Furthermore, IL-4 production by CLN and CSF cells was greatly enhanced when the cells were prepared from HSE mice previously treated with rIL-4. The IL-4 was mainly produced from CD4+ T cells. These results demonstrate that small amounts of exogenous IL-4 increase the severity of HSE in HSV-1-infected mice through the increased production of IL-4 from local CD4+ T cells.