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Myocardial Infarction Induces B Lymphopenia via a Mechanism Involving Cell Redistribution Between Peripheral Lymphoid Tissues and Bone Marrow
Author(s) -
Ma Yonggang,
Dickey Ann,
Chatterjee Victor,
Villalba Nuria,
Yang Xiaoyuan,
Yuan Sarah
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2021.35.s1.02484
Subject(s) - bone marrow , medicine , lymphocyte , spleen , lymphatic system , myocardial infarction , b cell , peripheral blood cell , pathology , lymph node , lymph , peripheral , immunology , antibody
Lymphopenia, a reduction in peripheral blood lymphocyte count, correlates with worse cardiac function and poor outcome in patients with myocardial infarction (MI) and is considered an independent prognostic biomarker. How it occurs after MI, however, is largely unknown. The objective of this study was to elucidate the underlying mechanisms by which MI drives B lymphopenia. Adult male C57BL/6J mice underwent permanent ligation of coronary artery to create MI and were sacrificed at days 1 and 3 post‐MI. Quantitative flow cytometric measurement revealed that blood B cell count dramatically decreased at days 1 and 3 post‐MI, compared to non‐MI controls, consistent with B lymphopenia. This was also confirmed in a mouse myocardial ischemia/reperfusion (I/R) model. The observation that MI did not increase apoptosis in blood B cells argues against apoptosis as the major contributing factor for MI‐induced B lymphopenia. We then investigated whether blood B cells migrate to and are retained in lymphoid organs. Similar to what was shown in the blood, the spleen and mesenteric lymph node in MI mice had lower mature B cell numbers and exhibited profound atrophy; in contrast, the bone marrow in post‐MI mice had more mature B cells than non‐MI controls, supporting that peripheral B cells travel to the bone marrow in response to MI. In conclusion, our study provides the first line of evidence suggesting that MI‐associated B lymphopenia involves B cell redistribution from peripheral lymphoid tissues to the bone marrow.