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Reports of Chagas disease are increasing in non-endemic populations across the globe. Apart from vector eradication and prevention efforts by public health organizations, current pharmacological interventions are sparse and show important side effects. In this issue of the BJP, Andrade et al. elegantly demonstrate a new pharmacological paradigm whereby Trypanosoma cruzi host cell invasion requires significant cross-talk between receptors for kinins and endothelins. It is shown, for example, that acting via both ETA and ETB receptors, endothelin-1 (ET-1) cooperates with the (TLR2/CXCR2/B2 kinin receptor) complex to activate inflammatory processes in response to invading trypomastigotes. This study by Andrade et al. prompts, however, several important questions, summarized in this Commentary, such as the putative role of chymase-dependent production of ET-1, the contentious protective role of ACE inhibitors in Chagasic patients, the unexplored role of de novo formed B1 receptors for kinins triggered by cytokines and the putative role of compartmentalized calcium pools in host cell invasion by trypomastigotes. LINKED ARTICLE This article is a commentary on Andrade et al., pp. 1333-1347 of this issue. To view this paper visit [ABSTRACT FROM AUTHOR]

A conference paper is presented that aims to determine whether the production of tumor necrosis factor (TNF)-α from monocytes due to Escherichia coli O157:H7 supernatant and purified verotoxins (VTs) could be modulated by the p38 kinase inhibitor SB203580. The study found that both E. coli O157 supernatant and VTs can upregulate the production of inflammatory cytokines such as TNF-α from monocytes and create a pro-inflammatory signal.

A conference paper is presented about the effect of bacterial stimulation on the production of interleukin (IL)-10 and transforming growth factor (TGF)-β and the effect of these cytokines, along with prostaglandin E2 (PGE2), on tumor necrosis factor-α levels in the human blood. The study found that the PGE2 is the most effective than IL-10 and TGF-β and it can endogenously control the level of IL-10. Furthermore, it showed that their interactions overlap with each other.

A conference paper about the levels of serum cytokine in male with proven coronary artery disease is presented. It aims to measure the serum cytokine levels in a cohort of 78 men with coronary artery disease. In doing so, the researchers had taken blood samples from the patients who undergone coronary angiography and who had a diagnosis of coronary artery disease. Results supported the connection of interleukin-1β in the development of coronary disease.