Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interleukin-7 (IL-7) and IL-8 productions in 25 children with acute rheumatic fever (ARF) and in 15 children with chronic rheumatic heart disease (CRHD) and in 15 children with streptococcal pharyngitis (SP), were investigated in order to determine whether they have a role in the pathogenesis of rheumatic fever. Significantly higher IL-8 levels were found in ARF patients in the clinically active period. IL-7 concentrations remained unchanged during different stages of rheumatic fever. The decrease of elevated IL-8 concentrations within 3 months and normal IL-8 concentrations in patients with CRHD and SP indicate an excessive production of IL-8, probably by cellular infiltrates in the joint throughout the active period of rheumatic disease.
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PMID:Plasma interleukin-7 (IL-7) and IL-8 concentrations in acute rheumatic fever and chronic rheumatic heart disease. 861 Feb 24

Group A streptococci (Streptococcus pyogenes or GAS) freshly isolated from individuals with streptococcal sore throat or invasive ("flesh-eating") infection often grow as mucoid colonies on primary culture but lose this colony appearance after laboratory passage. The mucoid phenotype is due to abundant production of the hyaluronic acid capsular polysaccharide, a key virulence determinant associated with severe GAS infections. These observations suggest that signal(s) from the human host trigger increased production of capsule and perhaps other virulence factors during infection. Here we show that subinhibitory concentrations of the human antimicrobial cathelicidin peptide LL-37 stimulate expression of the GAS capsule synthesis operon (hasABC). Up-regulation is mediated by the CsrRS 2-component regulatory system: it requires a functional CsrS sensor protein and can be antagonized by increased extracellular Mg(2+), the other identified environmental signal for CsrS. Up-regulation was also evident for other CsrRS-regulated virulence genes, including the IL-8 protease PrtS/ScpC and the integrin-like/IgG protease Mac/IdeS, findings that suggest a coordinated GAS virulence response elicited by this antimicrobial immune effector peptide. LL-37 signaling through CsrRS led to a marked increase in GAS resistance to opsonophagocytic killing by human leukocytes, an in vitro measure of enhanced GAS virulence, consistent with increased expression of the antiphagocytic capsular polysaccharide and Mac/IdeS. We propose that the human cathelicidin LL-37 has the paradoxical effect of stimulating CsrRS-regulated virulence gene expression, thereby enhancing GAS pathogenicity during infection. The ability of GAS to sense and respond to LL-37 may explain, at least in part, the unique susceptibility of the human species to streptococcal infection.
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PMID:Induction of group A Streptococcus virulence by a human antimicrobial peptide. 1893 85