Phagocytosis and oxycytosis: two arms of human innate immunity

Abstract

Human innate immunity operates in two compartments: extravascular (the tissues) and intravascular (the bloodstream). Physical conditions (fluid dynamics) in the compartments are different and, as a result, bactericidal mechanisms and involved cells are different as well. In relatively static media (the tissues, lymph nodes), bacteria are killed by phagocytes; in dynamic media (the bloodstream), bacteria are killed by erythrocytes. In the tissues and lymph nodes, resident macrophages and transmigrated from blood leukocytes (neutrophils and monocytes) recognize, engulf, kill, and digest bacteria; the clearance of the bloodstream from bacteria is performed by oxycytosis: erythrocytes catch bacteria by electric charge attraction and kill them by the oxygen released from oxyhemoglobin. Killed by erythrocytes, bacteria are decomposed and digested in the liver and the spleen. Phagocytosis by leukocytes in the tissues and oxycytosis by erythrocytes in the bloodstream are the main bactericidal mechanisms of human innate immunity.

α‐Haemolysin production, as a single factor, causes fulminant sepsis in a model ofEscherichia coli‐induced bacteraemia

“…Because HlyA certainly has the potential to change the behaviour or even lyse circulating immune active cells like monocytes (Fagerberg, Jakobsen, Skals, & Praetorius, ), the presence of HlyA could potentially interfere with intravascular bacterial clearance. Interestingly, the intravascular clearing of bacteria mechanistically has recently been argued to be markedly different from more solid tissues (for a review, see Minasyan, ). This review extracted documentation for the collective phagocytic system being too slow and having too low a capacity to effectively clear bacteria from the bloodstream.…”

“…Thus, the author argues for the erythrocyte as the main cell involved in intravascular bacterial clearance. The triboelectric charge of erythrocytes is mainly responsible for attracting and adhering of bacteria to erythrocytes, which are then able to kill the bacteria via its high oxygen content and release of reactive oxygen species (Minasyan, ). The ζ‐potential of the erythrocytes is mainly caused by sialic acid and can be markedly reduced by neuraminidase treatment (Munksgaard et al, ), but the ability of bacteria to adhere also depends on density, elasticity, and shape (Minasyan, ).…”

“…The triboelectric charge of erythrocytes is mainly responsible for attracting and adhering of bacteria to erythrocytes, which are then able to kill the bacteria via its high oxygen content and release of reactive oxygen species (Minasyan, ). The ζ‐potential of the erythrocytes is mainly caused by sialic acid and can be markedly reduced by neuraminidase treatment (Munksgaard et al, ), but the ability of bacteria to adhere also depends on density, elasticity, and shape (Minasyan, ). Interestingly, HlyA has an extreme impact on both the surface charge because HlyA causes immediate PS exposure in the outer leaflet (Fagerberg, Skals, Leipziger, & Praetorius, ; Skals et al, ) and a massive change in the overall shape of the erythrocyte (Skals et al, ), which is likely to affect bacterial clearance.…”

Predictive Factors and Microbial Spectrum for Infectious Complications after Hepatectomy with Cholangiojejunostomy in Perihilar Cholangiocarcinoma

“…Erythrocytes play an important role in human innate immunity. Bacteria in the bloodstream can be attracted and kept by erythrocytes and killed by oxidation [23,24]. There is no doubt that erythrocytopenia would undermine the protective mechanism.…”

The Broad-Ranging Panorama of Systemic Autoinflammatory Disorders With Specific Focus on Acute Painful Symptoms and Hematologic Manifestations in Children

“…In addition to being crucial for pathogen recognition through the mammalian cysteine protease caspase-1, a central enzyme of innate immunity, which processes pro-interleukin-1 (IL-1)β into the mature proinflammatory cytokine IL-1β, the discovery of monogenic and polygenic disorders in which inflammasome activity and IL-1 release are deregulated highlights the essential importance of inflammasome-supervised human defences against infections. 1 Different studies have demonstrated the existence of a functional hierarchy of proinflammatory cytokines in systemic autoinflammatory disorders (SAIDs), a heterogeneous cluster of rare genetically determined diseases involving innate immunity, mainly characterized by the recurrence of inflammatory flares affecting the skin, joints, serosal membranes, gastroenteric tube, central nervous system and other tissues, in which IL-1β is the most critical driver of inflammation at different levels. 2 , 3 The term “autoinflammatory” describes the nearly spontaneous appearance of inflammation in the almost complete absence of autoreactive T lymphocytes and/or specific autoantibodies and no clear evidence of infectious triggers.…”