Serum immunoglobulin levels, complement components 3 and 4, HLA-B27 allele and spondyloarthropathy in patients with non-infectious anterior uveites

Rives, Bárbara Torres; Téllez, Goitybell Martínez; Valdés, Minerva Matarán; Mesa, Teresa Collazo; González, Rosa Colás; Ambou, Isabel Frutos

doi:10.1016/j.reumae.2020.07.007

Cited by 1 publication

(2 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…They lack specificity but have expediency, which is critical for curbing the initial pathogen incursion. Subsequently, appropriate mechanisms need to be in place to curb prolonged complement activation 9 , 27 , 38 , 69 . Failure of these protective mechanisms has been demonstrated in several chronic diseases and in types of sepsis, but not in COVID-19 8 .…”

Section: Discussionmentioning

confidence: 99%

“…This suggests that cellular destruction would drive complement activation, especially if the complement protective markers are insufficient 8 , 9 , 50 . Correlation with RAGE and HMGB-1 may reflect that both markers are related to non-specific activation due to excessive necrosis and apoptosis, or are the DAMP, respectively 50 , 69 . Immune system activation is driven by several factors during COVID-19.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

A disturbed balance between blood complement protective factors (FH, ApoE) and common pathway effectors (C5a, TCC) in acute COVID-19 and during convalesce

Laudański

Okeke

Siddiq

et al. 2022

Sci Rep

View full text Add to dashboard Cite

A complement effect on homeostasis during infection is determined by both cytotoxic (activate complement component 5 (C5a) terminal cytotoxic complex (TCC)), and cytoprotective elements (complement factor H (FH), as well as apolipoprotein E (ApoE)). Here, we investigated the gap in knowledge in their blood milieu during SARS-CoV-2 infection with respect to the viral burden, level of tissue necrosis, and immunological response. 101 patients hospitalized with a PCR-confirmed diagnosis of COVID-19 had blood collected at H1 (48 h), H2 (3–4 Days), H3 (5–7 days), H4 (more than 7 days up to 93 days). Pre-existing conditions, treatment, the incidence of cerebrovascular events (CVA), a history of deep venous thrombosis (DVT) and pulmonary embolism (PE), and mortality was collected using electronic medical records. Plasma C5a, TCC, FH, and ApoE were considered as a complement milieu. Tissue necrosis (HMGB1, RAGE), non-specific inflammatory responses (IL-6, C-reactive protein), overall viral burden (SARS-CoV-2 spike protein), and specific immune responses (IgG, IgA, IgM directed αS- & N-proteins) were assessed simultaneously. C5a remained elevated across all time points, with the peak at 5–7 days. Studied elements of complement coalesced around three clusters: #0 (↑↑↑C5a, ↑↑TCC, ↓↓ApoE), #1 ↑C5a, ↑TCC, ↑↑↑FH); #2 (↑C5a, ↑TCC, ↑FH, ↑↑↑ApoE). The decline in FH and ApoE was a predictor of death, while TCC and C5a correlated with patient length of stay, APACHE, and CRP. Increased levels of C5a (Δ = 122.64; p = 0.0294; data not shown) and diminished levels of FH (Δ = 836,969; p = 0.0285; data not shown) co-existed with CVA incidence. C5a correlated storngly with blood RAGE and HMGB1, but not with viral load and immunological responsiveness. Remdesivir positively affected FH preservation, while convalescent plasma treatment elevated C5a levels. Three clusters of complement activation demonstrated a various milieu of ApoE & FH vs C5a & TCC in COVID-19 patients. Complement activation is linked to increased necrosis markers but not to viral burden or immune system response.

show abstract