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Although \u03b1<jats:sub>M<\/jats:sub>\u03b2<jats:sub>2<\/jats:sub>was extensively characterized and implicated in leukocyte inflammatory and immune functions, the roles of \u03b1<jats:sub>X<\/jats:sub>\u03b2<jats:sub>2<\/jats:sub>remain largely obscure. Here, we tested the ability of mice deficient in integrin \u03b1<jats:sub>M<\/jats:sub>\u03b2<jats:sub>2<\/jats:sub>or \u03b1<jats:sub>X<\/jats:sub>\u03b2<jats:sub>2<\/jats:sub>to deal with opportunistic infections and the capacity of cells derived from these animals to execute inflammatory functions. The absence of \u03b1<jats:sub>M<\/jats:sub>\u03b2<jats:sub>2<\/jats:sub>affected the recruitment of polymorphonuclear neutrophils (PMN) to bacterial and fungal pathogens as well as to model inflammatory stimuli, and \u03b1<jats:sub>M<\/jats:sub>\u03b2<jats:sub>2<\/jats:sub>-deficient PMN displayed defective inflammatory functions. In contrast, deficiency of \u03b1<jats:sub>X<\/jats:sub>\u03b2<jats:sub>2<\/jats:sub>abrogated intraperitoneal recruitment and adhesive functions of monocytes and macrophages (M\u03d5) and the ability of these cells to kill\/phagocytose<jats:named-content content-type=\"genus-species\">Candida albicans<\/jats:named-content>or<jats:named-content content-type=\"genus-species\">Escherichia coli<\/jats:named-content>cells both<jats:italic>ex vivo<\/jats:italic>and<jats:italic>in vivo<\/jats:italic>. During systemic candidiasis, the absence of \u03b1<jats:sub>X<\/jats:sub>\u03b2<jats:sub>2<\/jats:sub>resulted in the loss of antifungal activity by tissue M\u03d5 and inhibited the production of tumor necrosis factor alpha (TNF-\u03b1)\/interleukin-6 (IL-6) in infected kidneys. Deficiency of \u03b1<jats:sub>M<\/jats:sub>\u03b2<jats:sub>2<\/jats:sub>suppressed M\u03d5 egress from the peritoneal cavity, decreased the production of anti-inflammatory IL-10, and stimulated the secretion of IL-6. The absence of \u03b1<jats:sub>X<\/jats:sub>\u03b2<jats:sub>2<\/jats:sub>, but not of \u03b1<jats:sub>M<\/jats:sub>\u03b2<jats:sub>2<\/jats:sub>, increased survival against a septic challenge with lipopolysaccharide (LPS) by 2-fold. Together, these results suggest that \u03b1<jats:sub>M<\/jats:sub>\u03b2<jats:sub>2<\/jats:sub>plays a primary role in PMN inflammatory functions and regulates the anti-inflammatory functions of M\u03d5, whereas \u03b1<jats:sub>X<\/jats:sub>\u03b2<jats:sub>2<\/jats:sub>is central in the regulation of inflammatory functions of recruited and tissue-resident M\u03d5.<\/jats:p>","DOI":"10.1128\/iai.00644-16","type":"journal-article","created":{"date-parts":[[2016,11,1]],"date-time":"2016-11-01T01:12:21Z","timestamp":1477962741000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":39,"title":["Distinct Effects of Integrins \u03b1<sub>X<\/sub>\u03b2<sub>2<\/sub>and \u03b1<sub>M<\/sub>\u03b2<sub>2<\/sub>on Leukocyte Subpopulations during Inflammation and Antimicrobial Responses"],"prefix":"10.1128","volume":"85","author":[{"given":"Samir","family":"Jawhara","sequence":"first","affiliation":[{"name":"Department of Molecular Cardiology, Cleveland Clinic Lerner Research Institute, Cleveland, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elzbieta","family":"Pluskota","sequence":"additional","affiliation":[{"name":"Department of Molecular Cardiology, Cleveland Clinic Lerner Research Institute, Cleveland, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Cao","sequence":"additional","affiliation":[{"name":"Department of Molecular Cardiology, Cleveland Clinic Lerner Research Institute, Cleveland, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edward F.","family":"Plow","sequence":"additional","affiliation":[{"name":"Department of Molecular Cardiology, Cleveland Clinic Lerner Research Institute, Cleveland, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dmitry A.","family":"Soloviev","sequence":"additional","affiliation":[{"name":"Department of Molecular Cardiology, Cleveland Clinic Lerner Research Institute, Cleveland, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(02)00971-6"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-065X.1990.tb00565.x"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.R000004200"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M406968200"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.158.2.334"},{"key":"e_1_3_2_7_2","doi-asserted-by":"crossref","first-page":"3307","DOI":"10.4049\/jimmunol.134.5.3307","article-title":"Membrane complement receptor type three (CR3) has lectin-like properties analogous to bovine conglutinin as functions as a receptor for zymosan and rabbit erythrocytes as well as a receptor for iC3b","volume":"134","author":"Ross GD","year":"1985","unstructured":"Ross GD Cain JA Lachman PJ . 1985. 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