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Fulltext Pathophysiology of streptokinase-induced hypotension in acute myocardial infarction: a systematic review of clinical evidence

Khalid K, Ahmad RE, Tong AYH, Lui SY, Abidin IZZ

Arch Med Sci Atheroscler Dis, 2021;6:e85-e94.
PMID: 34027217 DOI: 10.5114/amsad.2021.105410

Introduction: Despite the common occurrence of streptokinase-induced hypotension among patients with acute myocardial infarction, the underlying pathophysiology remains obscure and poorly understood. Our study aimed to pool clinical evidence on the potential mechanism of streptokinase-induced hypotension through a systematic review of the literature.
Material and methods: We conducted literature search from Medline, Scopus and Web of Science on clinical studies related to streptokinase-induced hypotension.
Results: Our search yielded 972 citations. After removal of duplicates, 878 articles were screened for eligibility, of which 856 papers were excluded due to various reasons. Of the remaining 22 articles retrieved with full texts, eight relevant articles were selected for final analysis. Three themes emerged as the proposed mechanisms of streptokinase-induced hypotension, including (i) reduction in total peripheral resistance, (ii) complement activation, and (iii) dismissal of hypotheses involving other intermediaries.
Conclusions: Our findings suggest that the underlying mechanism of streptokinase-induced hypotension lies primarily in the reduction in total peripheral resistance.

Matched MeSH terms: Complement Activation
Fulltext Complement system specifically C5a receptor, inflammation and hypertrophic cardiomyopathy (HCM) in cats

Khor, K.H.

Jurnal Veterinar Malaysia, 2015;27(2):12-15.
MyJurnal

The complement cascade is a unique sequence of molecular events occurring within the vascular system in which inactive plasma proteins synthesised by the liver are activated following tissue injury (Figure ) (McGavin and Zachary, 2007). The increase permeability of blood vessels during inflammation is stimulated, at least in part, by the complement system. The complement system is a complex system of 30 serum proteins. Many early components are serine proteases that are activated sequentially to form a cascade. The complement cascade is activated through any one, or more, of four pathways: the classical, the mannan-binding lectin (MBL), the alternative and the extrinsic protease pathways (Guo and Ward, 2005; Monk et al., 2007; Ricklin and Lambris, 2007). For further information, refer (Manthey et al., 2009). (Copied from article)

Matched MeSH terms: Complement Activation
Fulltext Complement opsonization of HIV affects primary infection of human colorectal mucosa and subsequent activation of T cells

Bhattacharya P, Ellegård R, Khalid M, Svanberg C, Govender M, Keita ÅV, et al.

Elife, 2020 Sep 02;9.
PMID: 32876566 DOI: 10.7554/eLife.57869

HIV transmission via genital and colorectal mucosa are the most common routes of dissemination. Here, we explored the effects of free and complement-opsonized HIV on colorectal tissue. Initially, there was higher antiviral responses in the free HIV compared to complement-opsonized virus. The mucosal transcriptional response at 24 hr revealed the involvement of activated T cells, which was mirrored in cellular responses observed at 96 hr in isolated mucosal T cells. Further, HIV exposure led to skewing of T cell phenotypes predominantly to inflammatory CD4+ T cells, that is Th17 and Th1Th17 subsets. Of note, HIV exposure created an environment that altered the CD8+ T cell phenotype, for example expression of regulatory factors, especially when the virions were opsonized with complement factors. Our findings suggest that HIV-opsonization alters the activation and signaling pathways in the colorectal mucosa, which promotes viral establishment by creating an environment that stimulates mucosal T cell activation and inflammatory Th cells.

Matched MeSH terms: Complement Activation/immunology*
Fulltext Genome wide transcriptome profiling of a murine acute melioidosis model reveals new insights into how Burkholderia pseudomallei overcomes host innate immunity

Chin CY, Monack DM, Nathan S

BMC Genomics, 2010;11:672.
PMID: 21110886 DOI: 10.1186/1471-2164-11-672

At present, very little is known about how Burkholderia pseudomallei (B. pseudomallei) interacts with its host to elicit melioidosis symptoms. We established a murine acute-phase melioidosis model and used DNA microarray technology to investigate the global host/pathogen interaction. We compared the transcriptome of infected liver and spleen with uninfected tissues over an infection period of 42 hr to identify genes whose expression is altered in response to an acute infection.

Matched MeSH terms: Complement Activation/genetics
Relation of Doppler ultrasound synovitis versus clinical synovitis with changes in native complement component levels in rheumatoid arthritis patients treated with biologic disease-modifying anti-rheumatic drugs

Montoro Alvarez M, Chong OY, Janta I, González C, López-Longo J, Monteagudo I, et al.

Clin Exp Rheumatol, 2015 Mar-Apr;33(2):141-5.
PMID: 25665178

The complement system plays a fundamental role in mediating the activity of rheumatoid arthritis (RA). Biologic therapy can reduce native complement component levels and its activation. We aimed to study the relation of Doppler ultrasound (US) synovitis versus clinical synovitis with changes in native complement component levels in RA patients on biologic therapy.

Matched MeSH terms: Complement Activation/drug effects
Fulltext Genetic justification of severe COVID-19 using a rigorous algorithm

Gavriilaki E, Asteris PG, Touloumenidou T, Koravou EE, Koutra M, Papayanni PG, et al.

Clin Immunol, 2021 May;226:108726.
PMID: 33845193 DOI: 10.1016/j.clim.2021.108726

Recent studies suggest excessive complement activation in severe coronavirus disease-19 (COVID-19). The latter shares common characteristics with complement-mediated thrombotic microangiopathy (TMA). We hypothesized that genetic susceptibility would be evident in patients with severe COVID-19 (similar to TMA) and associated with disease severity. We analyzed genetic and clinical data from 97 patients hospitalized for COVID-19. Through targeted next-generation-sequencing we found an ADAMTS13 variant in 49 patients, along with two risk factor variants (C3, 21 patients; CFH,34 patients). 31 (32%) patients had a combination of these, which was independently associated with ICU hospitalization (p = 0.022). Analysis of almost infinite variant combinations showed that patients with rs1042580 in thrombomodulin and without rs800292 in complement factor H did not require ICU hospitalization. We also observed gender differences in ADAMTS13 and complement-related variants. In light of encouraging results by complement inhibitors, our study highlights a patient population that might benefit from early initiation of specific treatment.

Matched MeSH terms: Complement Activation