{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T02:11:06Z","timestamp":1790734266631,"version":"4.1.0"},"reference-count":50,"publisher":"BMJ","issue":"1","funder":[{"DOI":"10.13039\/100000053","name":"National Eye Institute","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000053","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["BMJ Open Ophth"],"accepted":{"date-parts":[[2017,10,20]]},"published-print":{"date-parts":[[2017,11]]},"abstract":"<jats:sec>\n                  <jats:title>Purpose<\/jats:title>\n                  <jats:p>The conjunctiva is a wet mucosal surface surrounding the cornea that is continuously exposed to pathogens. Nevertheless, persistent inflammation is not observed. We examined if the NOD-like receptor pyrin domain 3 (NLRP3) inflammasome functions as a sensor that distinguishes commensal and non-pathogenic bacteria from pathogenic bacteria in human conjunctival goblet cells.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>Goblet cells were grown from human conjunctiva and co-cultured with commensal <jats:italic>Staphylococcus epidermidis<\/jats:italic>, isogenic non-toxigenic <jats:italic>S. aureus<\/jats:italic> ACL135 and as a control toxigenic <jats:italic>S. aureus<\/jats:italic> RN6390. Activation of the NLRP3 inflammasome was determined by measuring changes in NF-\u03baB activity, expression of pro-interleukin (IL)-1\u03b2 and NLRP3, activation of caspase-1 and secretion of mature IL-1\u03b2. Goblet cell mucin secretion was measured in parallel.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>While all three strains of bacteria were able to bind to goblet cells, neither commensal <jats:italic>S. epidermidis<\/jats:italic> nor isogenic non-toxigenic <jats:italic>S. aureus<\/jats:italic> ACL135 was able to stimulate an increase in (1) NF-\u03baB activity, (2) pro-IL-1\u03b2 and NLRP3 expression, (3) caspase-1 activation, (4) mature IL-1\u03b2 and (5) mucin secretion. Toxigenic <jats:italic>S. aureus,<\/jats:italic> the positive control, increased these values: knockdown of NLRP3 with small interfering RNA (siRNA) completely abolished the toxigenic <jats:italic>S. aureus<\/jats:italic>-induced expression of pro-IL-1\u03b2 and secretion of mature IL-1\u03b2.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>We conclude that NLRP3 serves as a sensor capable of discriminating commensal and non-pathogenic bacteria from pathogenic bacteria in conjunctival goblet cells, and that activation of the NLRP3 inflammasome induced by pathogenic bacteria mediates secretion of both mature IL-1\u03b2 and large secretory mucins from these cells.<\/jats:p>\n               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