The macrophage: Past, present and future

Gordon, Siamon

doi:10.1002/eji.200737638

Cited by 508 publications

(409 citation statements)

References 80 publications

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“…This suggests that CD11b is far more important in monocyte recruitment to infected tissues than it is to controlling infection within tissues, when cells have differentiated into functional myeloid-derived effector cells. As monocytes are not as efficient in performing the effector functions of macrophages, including phagocytosis of dead cells (62,63), it is possible that propofol exposure resulted in the uncontrolled expansion of neutrophilic abscesses as a result of reduced macrophage populations and the associated reduction in the phagocytosis of neutrophil corpses. In addition to the drug's potential effects on monocyte differentiation, in vitro studies have shown that exposure to propofol decreases phagocytosis of latex beads in human microglial cell culture (64) and in human THP-1 macrophage cell lines (26).…”

Section: Discussionmentioning

confidence: 99%

Propofol Sedation Exacerbates Kidney Pathology and Dissemination of Bacteria during Staphylococcus aureus Bloodstream Infections

Visvabharathy

Freitag

2017

Infect Immun

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Methicillin-resistant Staphylococcus aureus (MRSA) is responsible for large numbers of postsurgical nosocomial infections across the United States and worldwide. Propofol anesthesia is widely used in surgery and in intensive care units, and recent evidence indicates that even brief exposure to propofol can substantially increase host susceptibility to microbial infection. Here, we delineate the impact of propofol sedation on MRSA bloodstream infections in mice in the presence and absence of prophylactic antibiotic treatment. Consistent with previous reports, brief periods of anesthesia with propofol were sufficient to significantly increase bacterial burdens and kidney pathology in mice infected with MRSA. Propofol exposure increased neutrophilic infiltrates into the kidney and enhanced bacterial dissemination throughout kidney tissue. Propofol sedation reduced populations of effector phagocytes and mature dendritic cells within the kidney and led to the apparent expansion of myeloid-derived suppressor cell-like populations. When propofol was coadministered with vancomycin prophylaxis, it dramatically increased kidney abscess formation and bacterial dissemination throughout kidney tissue at early times post-S. aureus infection compared to antibiotic-treated but nonsedated animals. Taken together, our data indicate that short-term sedation with propofol significantly increases the severity of bloodstream MRSA infection, even when administered in conjunction with vancomycin prophylaxis.KEYWORDS MRSA, anesthesia, bacterial pathogenesis, immune suppression, kidney abscess, macrophages, monocytes, vancomycin N osocomial infections are common complications that follow surgery or prolonged stays in intensive care units (ICU) of hospitals (1-5) and which result in large increases in patient morbidity and mortality in addition to elevated health care costs (6). The causative agents of nosocomial infection are often bacteria (4, 7), and Staphylococcus aureus is one of the most frequently isolated pathogens in this regard (8). Antibiotic treatment of S. aureus infections can be complicated by the prevalence of methicillin-resistant S. aureus (MRSA) strains in hospitals and increasingly in community settings (9, 10). Patients often require multiple antibiotics or use of broad-spectrum antibiotics to eradicate infection (11). Despite numerous measures taken to ensure sterility and limit spread of MRSA from health care workers to patients in hospitals (12, 13), the rate of infection remains high (14,15). While significant effort is generally focused on enforcing aseptic technique as a method to prevent infection, there may be additional factors that influence the frequency and/or severity of nosocomial infections (16).Propofol is one of the most common anesthetic agents used in the induction and maintenance of anesthesia prior to surgery, both in the intensive care unit (ICU) and in routine outpatient procedures (17)(18)(19)(20). This is in part due to its low incidence of anesthesia-related side effects and the shor...

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Section: Discussionmentioning

confidence: 99%

Propofol Sedation Exacerbates Kidney Pathology and Dissemination of Bacteria during Staphylococcus aureus Bloodstream Infections

Visvabharathy

Freitag

2017

Infect Immun

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“…SP-D связывается с грамотрицательными бактериями, такими как Pseudomonas aeruginosa, Klebsiella pneumoniae, Escherichia coli и Haemophilus influenzaе, способствуя их агглютинации и стимуляции хемотак-сиса нейтрофилов, макрофагов и эозинофилов к месту инвазии патогена [25][26][27]. SP-D также может связываться с грамположи-тельными бактериями, такими как Streptococcus pneumoniae и Stafylococcus aureus, а также с микобактериями [28,29], респира-торно-синцитиальным вирусом, вирусом гриппа [30], грибами Pneumocystis carinii, Aspergillus fumigatus, Cryptococcus neoformans, Candida albicans [31].…”

Section: терапевтический архив 1 2015unclassified

Significance of surfactant proteins in the diagnosis of therapeutic diseases

et al. 2015

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“…However, macrophages can also be stimulated by signals induced by other antigen-specific immune cells [37]. These signals produced by these specific immune cells are very clear, strong, and long lasting, which lead to alteration in macrophages for a very long period of time [42].…”

Section: Macrophages and Cancermentioning

confidence: 99%

Adenosine as an endogenous immunoregulator in cancer pathogenesis: where to go?

Kumar

2012

Purinergic Signalling

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Cancer is a chronic disease and its pathogenesis is well correlated with infection and inflammation. Adenosine is a purine nucleoside, which is produced under metabolic stress like hypoxic conditions. Acute or chronic inflammatory conditions lead to the release of precursor adenine nucleotides (adenosine triphosphate (ATP), adenosien diphosphate (ADP) and adenosine monophosphate (AMP)) from cells, which are extracellularly catabolized into adenosine by extracellular ectonucleotidases, i.e., CD39 or nucleoside triphosphate dephosphorylase (NTPD) and CD73 or 5′-ectonucleotidase. It is now well-known that adenosine is secreted by cancer as well as immune cells during tumor pathogenesis under metabolic stress or hypoxia. Once adenosine is released into the extracellular environment, it exerts various immunomodulatory effects via adenosine receptors (A 1 , A 2A , A 2B , and A 3 ) expressed on various immune cells (i.e., macrophages, myeloid-derived suppressor cells (MDSCs), natural killer (NK) cells, dendritic cells (DCs), T cells, regulatory T cell (T regs ), etc.), which play very important roles in the pathogenesis of cancer. This review is intended to summarize the role of inflammation and adenosine in the immunopathogenesis of tumor along with regulation of tumor-specific immune response and its modulation as an adjunct approach to tumor immunotherapy.

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The macrophage: Past, present and future

Cited by 508 publications

References 80 publications

Propofol Sedation Exacerbates Kidney Pathology and Dissemination of Bacteria during Staphylococcus aureus Bloodstream Infections

Propofol Sedation Exacerbates Kidney Pathology and Dissemination of Bacteria during Staphylococcus aureus Bloodstream Infections

Significance of surfactant proteins in the diagnosis of therapeutic diseases

Adenosine as an endogenous immunoregulator in cancer pathogenesis: where to go?

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