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Inflammation triggered during pneumonia is necessary for bacterial clearance but must be spatially and temporally regulated to prevent further tissue damage and bacterial dissemination. Emerging data shows that annexin A1 (ANXA1) signalling through its receptor FPR2 promotes host resistance and resilience in preclinical models of infectious disease.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>\n                      Using a mouse model of\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>Escherichia coli<\/jats:italic>\n                      <\/jats:styled-content>\n                      \u2010induced pneumonia, the role of ANXA1\/FPR2 on key steps of inflammation resolution was evaluated.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Anxa1<\/jats:italic>\n                      and\n                      <jats:italic>Fpr2\/3<\/jats:italic>\n                      knockout mice, intranasally infected with\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>E. coli<\/jats:italic>\n                      <\/jats:styled-content>\n                      <jats:italic>,<\/jats:italic>\n                      exhibited exacerbated neutrophilic inflammation, higher bacterial dissemination, decreased neutrophil apoptosis\/efferocytosis counts in the airways and higher levels of inflammatory cytokines\/chemokines coupled to marked lung damage and dysfunction, as compared to WT mice. Treatment of WT\u2010infected mice with the ANXA1 peptidomimetic, annexin I\u2010(2\u201026), decreased inflammation, increased apoptosis\/efferocytosis of neutrophils and improved bacterial clearance in the airways and lungs, resulting in an improvement of lung function. The pan\u2010caspase inhibitor Z\u2010VAD\u2010FMK prevented annexin I\u2010(2\u201026)\u2010induced resolution of the neutrophilic inflammation, underlining neutrophil apoptosis as the main mechanism for annexin I\u2010(2\u201026) promotion of resolution of\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>E. coli<\/jats:italic>\n                      <\/jats:styled-content>\n                      pneumonia. In addition, annexin I\u2010(2\u201026) treatment increased the numbers of airway macrophages of infected mice and promoted macrophage phagocytosis of\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>E. coli<\/jats:italic>\n                      <\/jats:styled-content>\n                      <jats:italic>in vitro<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and Implications<\/jats:title>\n                    <jats:p>\n                      In summary, these findings highlight the role for ANXA1\/FPR2 pathway as a nonredundant resolution mechanism for\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>E. coli<\/jats:italic>\n                      <\/jats:styled-content>\n                      <jats:italic>\u2010<\/jats:italic>\n                      induced pneumonia and demonstrate that annexin I\u2010(2\u201026) as a potential host\u2010directed therapeutic approach to treat infectious lung diseases.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.70026","type":"journal-article","created":{"date-parts":[[2025,4,3]],"date-time":"2025-04-03T22:23:09Z","timestamp":1743718989000},"page":"3539-3558","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Annexin A1\/FPR2 pathway modulates leukocyte function during\n                    <scp>\n                      <i>Escherichia coli<\/i>\n                    <\/scp>\n                    \u2010induced pneumonia to promote resolution of inflammation and restores lung function"],"prefix":"10.1111","volume":"182","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-6791-2189","authenticated-orcid":false,"given":"Edvaldo 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