Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0220723 (PCA)
4,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

IgE levels in the bronchoalveolar lavage fluids (BALF) of rats increased significantly following infection with Nippostrongylus brasiliensis. This increase corresponded with a concurrent increase in serum IgE levels. However, a comparison of IgE to albumin ratio in both BALF and serum suggested local accumulation and/or production of IgE in the bronchoalveolar spaces rather than leakage from serum. Subsequent analysis of BALF showed presence of heat-labile PCA activity with highest anti-worm titer (1:64) on Days 11-16 postinfection (pi). Secondary infection resulted in up to a fourfold increase in PCA activity compared to primary infection. Immunoblot analysis showed that these parasite-specific IgE antibodies in BALF recognized many proteins of adult worms ranging from 16-290 kDa. IgE antibodies in serum and BALF showed similarities in their reactivities toward adult worm antigens. However, the IgE antibody reactivities to different antigens varied significantly among different days pi. Depletion of IgG from BALF and serum resulted in more intense binding by IgE antibodies to antigens than when IgG was not depleted. Concurrent with the elevated levels of IgE antibodies, there was a significant increase in the levels of histamine in BALF, suggesting activation of mast cells. Thus, following N. brasiliensis infection there is an abundance of parasite-specific IgE antibodies in the lower respiratory tract and IgE-mediated pathways of inflammation appeared to be activated in the lungs.
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PMID:IgE antibody responses in bronchoalveolar spaces of rats infected with Nippostrongylus brasiliensis. 846 97

Using a murine model, we have demonstrated the establishment of cerebral resistance to local lethal challenge with Candida albicans strain CA-6, by previous intracerebral (i.c.) infection with the low-virulent strain PCA-2. Here we show that i.c. infection with PCA-2 is effective in drastically reducing brain colonization following secondary infection with CA-6. As assessed by colony forming unit assay and histopathological analysis, microbial counts are impaired, granuloma formation and hyphal growth are also reduced in brains of PCA-2- and CA-6-infected mice with respect to CA-6-challenged mice. Furthermore, using PCR studies, we found that, while PCA-2 (i.e. healing infection) induces transient cytokine gene expression in the mouse brain, CA-6 lethal challenge results in long-lasting (until mouse death) high levels of all cytokine gene transcripts assessed. Finally brains from mice that will resist CA-6 challenge, because of previous infection with PCA-2, also exhibit a transient induction of all cytokine genes. Only IL-1 beta remains highly expressed at all time- points tested. Overall, these results provide evidence that healing and non-healing C. albicans i.c. infections differ in the immune reaction(s) locally evoked, at least in terms of cytokine gene expression, strongly suggesting cytokine involvement in the establishment of brain anticandidal resistance.
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PMID:Biomolecular events involved in the establishment of brain anticandidal resistance. 859 94