Abstract
Neutrophil mobilization is a crucial response to protect the host against invading microorganisms. Neutrophil recruitment and removal have to be tightly regulated to prevent uncontrolled inflammation and excessive release of their toxic content causing tissue damage and subsequent organ dysfunctions. We show here the presence of live and apoptotic neutrophils in the cytoplasm of inflamed mammary, urinary and gall bladder epithelial cells following infection with E. coli and Salmonella bacteria. The entry process commenced with adherence of transmigrated neutrophils to the apical membrane of inflamed epithelial cells. Next, nuclear rearrangement and elongation associated with extensive actin polymerization enabled neutrophils to crawl and invaginate the apical membrane into cytoplasmic double membrane compartments. Scission of the invaginated cell membrane from the entry point and loss of these surrounding membranes released intracellular neutrophils into the cytoplasm where they undergone apoptotic death. The co-occurrence of this observation with bacterial invasion and formation of intracellular bacterial communities (IBCs) might link entry of infected neutrophils to the formation of IBCs and chronic carriage in E. coli mastitis and cystitis and Salmonella cholecystitis.
Highlights
Massive recruitment of blood neutrophils to sites of infection is the hallmark of many diseases [1]
intracellular bacterial communities (IBC) of urinary pathogenic E. coli (UPEC) in bladder epithelial cells were described in mouse urinary tract infection (UTI) model and naturally infected women [15, 16], and are shown here following trans-urethral ascending infection (Figure 2)
Nuclear rearrangement and elongation was associated with extensive actin polymerization that enabled neutrophils to crawl and invaginate the apical membrane into cytoplasmic double membrane compartments
Summary
Massive recruitment of blood neutrophils to sites of infection is the hallmark of many diseases [1]. Safe disposal and clearance of recruited neutrophils is essential to prevent host-tissue injury and progression of disease. This is achieved by three known mechanisms; (1) migration and mobilization to the lumen of epithelial-lined structures (e.g. urine, milk, bile, bronchi, gut) (2) reverse migration into blood, and (3) phagocytosis or efferocytosis by macrophages [2,3,4]. Resident and mobilized macrophages are frequently described as major contributors to phagocytosis and intracellular elimination of dying neutrophils while eliciting anti-inflammatory cytokines [5, 6] This notion is based on many studies using peritonitis, air pouch or pneumonia mouse models, where abundant mobilization of blood monocytes or tissue macrophages is typically observed. In some tissues and disease processes macrophages may not be sufficient
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