D S Heffernan1, S F Monaghan2, Alfred Ayala2. 1. Division of Surgical Research, Department of Surgery, Warren Alpert Medical School of Brown UniversityRhode Island Hospital, 211 Aldrich Building, 593 Eddy Street, Providence, 02903, RI, USA. DHeffernan@Brown.edu. 2. Division of Surgical Research, Department of Surgery, Warren Alpert Medical School of Brown UniversityRhode Island Hospital, 211 Aldrich Building, 593 Eddy Street, Providence, 02903, RI, USA.
Abstract
BACKGROUND: Systemic Inflammatory Response Syndrome (SIRS) and sepsis remain leading causes of death. Despite many similarities, the two entities are very distinct clinically and immunologically. T-Lymphocytes play a key pivotal role in the pathogenesis and ultimately outcome following both SIRS and sepsis. Integrins are essential in the trafficking and migration of lymphocytes. They also serve vital roles in efficient wound healing and clearance of infections. Here, we investigate whether integrin expression, specifically β1 (CD29) and β2 (CD18), are disrupted in SIRS and sepsis, and assess differences in integrin expression between these two critically ill clinical categories. METHODS: T-Lymphocytes were isolated from whole blood collected from ICU patients exhibiting SIRS or sepsis. Samples were analyzed for CD18 (β2) and CD29 (β1) on CD3+ T cells through flow cytometry. Septic patients were stratified into either exclusively abdominal or non-abdominal sources of sepsis. RESULTS: CD18 was almost ubiquitously expressed on CD3+ T cells irrespective of clinical condition. However, CD29 (β1 integrin) was lowest in SIRS patients (20.4% of CD3+ T cells) when compared with either septic patients (35.5%) or healthy volunteers (54.1%). Furthermore, there was evidence of compartmentalization in septic patients, where abdominal sources had a greater percentage of CD3+CD29+ T cells (41.7%) when compared with those with non-abdominal sources (29.5%). CONCLUSION: Distinct differences in T-cell integrin expression exists between patients in SIRS versus sepsis, as well as relative to the source of sepsis. Further work is needed to understand cause and effect relative to the progression from SIRS into sepsis.
BACKGROUND: Systemic Inflammatory Response Syndrome (SIRS) and sepsis remain leading causes of death. Despite many similarities, the two entities are very distinct clinically and immunologically. T-Lymphocytes play a key pivotal role in the pathogenesis and ultimately outcome following both SIRS and sepsis. Integrins are essential in the trafficking and migration of lymphocytes. They also serve vital roles in efficient wound healing and clearance of infections. Here, we investigate whether integrin expression, specifically β1 (CD29) and β2 (CD18), are disrupted in SIRS and sepsis, and assess differences in integrin expression between these two critically ill clinical categories. METHODS: T-Lymphocytes were isolated from whole blood collected from ICU patients exhibiting SIRS or sepsis. Samples were analyzed for CD18 (β2) and CD29 (β1) on CD3+ T cells through flow cytometry. Septicpatients were stratified into either exclusively abdominal or non-abdominal sources of sepsis. RESULTS:CD18 was almost ubiquitously expressed on CD3+ T cells irrespective of clinical condition. However, CD29 (β1 integrin) was lowest in SIRS patients (20.4% of CD3+ T cells) when compared with either septicpatients (35.5%) or healthy volunteers (54.1%). Furthermore, there was evidence of compartmentalization in septicpatients, where abdominal sources had a greater percentage of CD3+CD29+ T cells (41.7%) when compared with those with non-abdominal sources (29.5%). CONCLUSION: Distinct differences in T-cell integrin expression exists between patients in SIRS versus sepsis, as well as relative to the source of sepsis. Further work is needed to understand cause and effect relative to the progression from SIRS into sepsis.
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Authors: Nicholas J Shubin; Sean F Monaghan; Daithi S Heffernan; Chun-Shiang Chung; Alfred Ayala Journal: Crit Care Date: 2013-11-29 Impact factor: 9.097