Use of complement regulators, CD35, CD46, CD55, and CD59, on leukocytes as markers for diagnosis of viral and bacterial infections

Nuutila, Jari; Jalava-Karvinen, Päivi; Hohenthal, Ulla; Kotilainen, Pirkko; Pelliniemi, Tarja‐Terttu; Nikoskelainen, J; Lilius, Esa‐Matti

doi:10.1016/j.humimm.2013.01.011

Cited by 28 publications

(31 citation statements)

References 27 publications

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“…CR1 on neutrophils binds C3b-opsonized particles and facilitates phagocytosis by stimulating CR3 and CR4 [47]. Expression of CR1 on neutrophils is increased upon stimulation [48], especially during a bacterial infection [49]. The importance of CR1 for phagocytosis in vivo is demonstrated in a mouse model where loss of CR1 strongly contributed to survival of S .…”

Section: Discussionmentioning

confidence: 99%

Staphylococcal protein Ecb impairs complement receptor-1 mediated recognition of opsonized bacteria

et al. 2017

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Staphyloccus aureus is a major human pathogen leading frequently to sepsis and soft tissue infections with abscesses. Multiple virulence factors including several immune modulating molecules contribute to its survival in the host. When S. aureus invades the human body, one of the first line defenses is the complement system, which opsonizes the bacteria with C3b and attract neutrophils by release of chemotactic peptides. Neutrophils express Complement receptor-1 [CR1, CD35) that interacts with the C3b-opsonized particles and thereby plays an important role in pathogen recognition by phagocytic cells. In this study we observed that a fraction of S. aureus culture supernatant prevented binding of C3b to neutrophils. This fraction consisted of S. aureus leukocidins and Efb. The C-terminus of Efb is known to bind C3b and shares significant sequence homology to the extracellular complement binding protein [Ecb). Here we show that S. aureus Ecb displays various mechanisms to block bacterial recognition by neutrophils. The presence of Ecb blocked direct interaction between soluble CR1 and C3b and reduced the cofactor activity of CR1 in proteolytic inactivation of C3b. Furthermore, Ecb could dose-dependently prevent recognition of C3b by cell-bound CR1 that lead to impaired phagocytosis of NHS-opsonized S. aureus. Phagocytosis was furthermore reduced in the presence of soluble CR1 [sCR1). These data indicate that the staphylococcal protein Ecb prevents recognition of C3b opsonized bacteria by neutrophil CR1 leading to impaired killing by phagocytosis and thereby contribute to immune evasion of S. aureus.

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Section: Discussionmentioning

confidence: 99%

Staphylococcal protein Ecb impairs complement receptor-1 mediated recognition of opsonized bacteria

et al. 2017

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“…Active neutrophils express cell surface CR1 (CD35) and CR3 (CD11b/CD18) that are essential for their transmigration to protect the host against invading microorganisms [33]. Increase in membrane-bound CD35 [12] and CD11b [34], [35] in both neutrophils and monocytes has been reported following bacterial and viral infections, especially the latter [35]. In fact, CD35 expression on neutrophils and monocytes is considered effective markers of bacterial infection [12].…”

Section: Discussionmentioning

confidence: 99%

“…Increase in membrane-bound CD35 [12] and CD11b [34], [35] in both neutrophils and monocytes has been reported following bacterial and viral infections, especially the latter [35]. In fact, CD35 expression on neutrophils and monocytes is considered effective markers of bacterial infection [12]. Neutrophil influx from blood to the tissues is driven in large part by interleukin-8, a strong neutrophil chemoattractant.…”

Section: Discussionmentioning

confidence: 99%

“…Monocyte subsets were defined based on surface expression of CD14 and CD16 [12], [13]. Briefly, whole blood samples (25 μL) anticoagulated with K3EDTA were incubated with the saturating concentration of PE-conjugated mouse antihuman CD16 and FITC-conjugated antihuman CD14 (Becton Dickinson) for 30 minutes in the darkness.…”

Section: Methodsmentioning

confidence: 99%

“…Infections, mostly due to bacterial and viral origin, induce different expression patterns of complement regulators in the human leukocyte membrane. For example, an increase in membrane-bound CD35 on neutrophils and monocytes is a strong marker of bacterial infection [12].…”

Section: Introductionmentioning

confidence: 99%

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Alteration in Leukocyte Subsets and Expressions of FcγR and Complement Receptors among Female Ragpickers in Eastern India

Mondal

Siddique

Banerjee

et al. 2017

Safety and Health at Work

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BackgroundThere are a million ragpickers in India who gather and trade recyclable municipal solid wastes materials for a living. The objective of this study was to examine whether their occupation adversely affects their immunity.MethodsSeventy-four women ragpickers (median age, 30 years) and 65 age-matched control housemaids were enrolled. Flow cytometry was used to measure leukocyte subsets, and leukocyte expressions of Fcγ receptor I (CD64), FcγRIII (CD16), complement receptor 1 (CD35) and CR3 (CD11b/CD18), and CD14. Serum total immunoglobulin-E was estimated with enzyme-linked immunosorbent assay.ResultsCompared with the controls, ragpickers had significantly (p < 0.0001) higher levels of CD8+T-cytotoxic, CD16+CD56+natural killer, and CD4+CD45RO+memory T-cells, but depleted levels of CD19+B-cells. The percentage of CD4+T-helper-cells was lower than the control group (p < 0.0001), but their absolute number was relatively unchanged (p = 0.42) due to 11% higher lymphocyte counts in ragpickers. In ragpickers, the percentages of CD14+CD16+intermediate and CD14dim CD16+nonclassical monocyte subsets were elevated with a decline in CD14+CD16-classical monocytes. The expressions of CD64, CD16, CD35, and CD11b/CD18 on both monocytes and neutrophils, and CD14 on monocytes were significantly higher in ragpickers. In addition, ragpickers had 2.7-times more serum immunoglobulin-E than the controls (p < 0.0001). After controlling potential confounders, the profession of ragpicking was positively associated with the changes.ConclusionRagpicking is associated with alterations in both innate (neutrophils, monocytes, and natural killer cell numbers and expression of complement and Fcγ receptors) and adaptive immunity (numbers of circulating B cells, helper, cytotoxic, and memory T cells).

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Low-level arsenic causes chronic inflammation and suppresses expression of phagocytic receptors

Prasad

Sinha

2017

Environ Sci Pollut Res

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The impact of chronic low-level groundwater arsenic (As) exposure [in the range above the WHO-recommended limit of 10 μg/L but ≤50 μg/L (permissible limit of As for many Asian countries)] was investigated for cross talk of inflammatory changes and expression of phagocytic receptors of exposed rural women (N, 45) from districts of 24 Parganas (south) and in matched control groups (N, 43) [As ≤10 μg/L] from the same district. Systemic inflammation was evident from the upregulated levels of pro-inflammatory mediators like tumor necrosis factor-α (TNF-α); interleukins (ILs) like IL-6, IL-8, and IL-12; and C-reactive protein (CRP) in the sera and upregulated expression of protein kinase B phosphorylated at ser473 (pAKTser473)/nuclear factor-κB (NF-κB)/TNF-α axis in the leukocytes of exposed women with respect to control. We found that low-dose As exposure apart from inflicting inflammation altered the expression of phagocytic receptors-Fcγ receptors (FcγRs) and complement receptors (CRs). The leukocytes of the low-As-exposed women exhibited suppression of CD64, CD35, and CD11b and increased expression of CD16 with respect to control. Groundwater As showed a negative correlation with CD64 expression on monocytes [Pearson's r, -0.8205; 95% confidence interval (CI), -0.8789 to -0.7379] and granulocytes [r, -0.7635; 95% CI, -0.8388 to -0.6595] and a positive correlation with CD16 on granulocytes [r, 0.8363; 95% CI, 0.7599 to 0.8899]. A negative correlation of groundwater As was also observed with expression of CD35 on granulocytes [r, -0.8780; 95% CI, -0.9185 to -0.8192] and monocytes [r, -0.7778; 95% CI, -0.8490 to -0.6790] and CD11b on monocytes [r, -0.6035; 95% CI, -0.7218 to -0.4511]. Therefore, it may be indicated that chronic low-level As exposure (11-50 μg/L) not only evoked chronic inflammatory changes but also suppressed the expression of FcγRs and CRs in the exposed women. This, in turn, may lead to susceptibility towards pathogenic infections or in long run may even contribute towards chronic inflammatory diseases including cancer.

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Use of complement regulators, CD35, CD46, CD55, and CD59, on leukocytes as markers for diagnosis of viral and bacterial infections

Cited by 28 publications

References 27 publications

Staphylococcal protein Ecb impairs complement receptor-1 mediated recognition of opsonized bacteria

Staphylococcal protein Ecb impairs complement receptor-1 mediated recognition of opsonized bacteria

Alteration in Leukocyte Subsets and Expressions of FcγR and Complement Receptors among Female Ragpickers in Eastern India

Low-level arsenic causes chronic inflammation and suppresses expression of phagocytic receptors

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