PubMed · 8012532
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V L Bykov. [Solid cell nests in the human thyroid].. https://pubmed.ncbi.nlm.nih.gov/8012532/
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Human peritoneal mesothelial cells (HPMC) respond to tumor necrosis factor alpha (TNF alpha) by releasing various cytokines that may activate the endothelium and induce recruitment of leukocytes during peristonitis. We characterized the receptors for TNF on HPMC to elucidate their functions in peritonitis. Scatchard analysis determined the presence of 70 x 10(3) TNF receptors/cell with a kDa of 0.44 nM. TNF receptor 1 (TNF-R1, p55) and TNF-R2 (p75) mRNA were demonstrated by reverse-transcriptase-PCR (RT-PCR). TNF-R1 protein was solely detected by flow cytometry (FCM). Interleukin-1 alpha (IL-1 alpha) induced down-regulation of TNF-R1. This was concomitant with accumulation of soluble TNF-R1 (sTNF-R1) detected by specific ELISA. LPS had a lower TNF-R1-shedding activity while TNF alpha did not induce shedding. The IL-1-induced-sTNF-R1-shedding was suppressed by the protein-kinase-A (PKA) inhibitor, H-8, or by H-7, the inhibitor of both PKC and PKA, but not by the specific PKC inhibitor GF. These experiments suggest a role for PKA in the IL-1-shedding signal. No change in TNF-R1 mRNA levels was observed after IL-1 alpha or TNF alpha stimulation while TNF-R2 (p75) mRNA basal levels transiently increased three to fivefold, reaching a peak after four hours followed by an accumulation of sTNF-R2 in the supernatant. Our data suggest that the main receptor expressed on HPMC is TNF-R1. Down-regulation and shedding of TNF-R1 induced by IL-1, and the transient expression of TNF-R2 induced by IL-1 and TNF, may regulate the responses to TNF by HPMC. These results may be important in understanding the inflammatory process of peritonitis were TNF plays a major role.
The study was carried out to determine the role of lectins and sugars in the adhesion of S. pyogenes to human pharyngeal and buccal epithelial cells. In vitro adhesion assay has shown that Con A and Dolicos biflorus lectins inhibited the attachment of S. pyogenes to the oropharyngeal mucosal cells. Among different sugars used, N-acetyl-D-galactosamine and D-galactose have significantly blocked the binding of streptococci to PEC and BEC. These findings indicate that lectins and sugar molecules mediate the adhesion of S. pyogenes to the pharyngeal epithelial cells which may be important in the cellular pathogenesis of streptococcal infections which originate at the human oropharyngeal mucosa.
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