Innate inflammatory response to acute inhalation exposure of riot control agent oleoresin capsicum in female rats: An interplay between neutrophil mobilization and inflammatory markers

2020 ◽  
Vol 46 (3-4) ◽  
pp. 81-97
Author(s):  
Pompy Patowary ◽  
Manash Pratim Pathak ◽  
Kamaruz Zaman ◽  
Sanjai Kumar Dwivedi ◽  
Pronobesh Chattopadhyay
2020 ◽  
Vol 27 (1) ◽  
pp. 16-24
Author(s):  
Marcelo G. Lima ◽  
Vitor S. Tardelli ◽  
Elisa Brietzke ◽  
Thiago M. Fidalgo

<b><i>Introduction:</i></b> Although the recreational cannabis use is expressive worldwide, the literature about medical potential of cannabis extracts, including its anti-inflammatory properties, remains inconclusive. <b><i>Methods:</i></b> We screened all articles, published on the PubMed database, on inflammatory mediators and any information about cannabis use from 1980 to March 2019. <b><i>Results:</i></b> Six studies were included, and the main findings were as follows: (i) among healthy volunteers and cannabis users, cannabinoids seemed to decrease the inflammatory response, thus decreasing the immune response, which led to a higher risk of infections; (ii) among patients with multiple sclerosis, cannabinoids seemed to have little impact on the inflammatory markers’ levels. <b><i>Discussion:</i></b> Although cannabis use can produce immune inflammatory suppression in healthy people, this effect is not robust enough to change inflammatory mediators’ levels in situations of highly dysfunctional inflammatory activation. Nevertheless, the impact of cannabinoids in clinical outcomes of these conditions remains to be determined.


2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Fei Ge ◽  
Haoran Yang ◽  
Weiting Lu ◽  
Huilian Shi ◽  
Qinlei Chen ◽  
...  

Perimenopausal women are associated with increased risks of depression and anxiety, which may be potentially related to the lack of ovarian hormone with antidepression activity in the body. However, the precise mechanism remains unclear so far. This study first adopted the Sprague-Dawley (SD) female rats to construct the ovariectomy (OVX) combined with a chronic unpredictable stress (CUS) model. Then, a series of behavioral experimental results revealed that the ovariectomized rats receiving CUS had remarkably elevated anxiety and depression behaviors relative to those in sham group rats, and the sucrose preference rate in the sucrose preference test (SPT) was evidently reduced. In elevated plus maze test (EPM) experiment, the open arm entry time and open arm duration were decreased. In the open field test (OFT), the number of line crossings, rearing number, center square entries, and center square duration were reduced; the grooming time was extended; and the number of fecal particles in rats was increased. In the forced swimming test (FST), the rat immobility rate was increased, while the numbers of swimming and crawling were decreased. Afterwards, we discovered that OVX downregulated the serum levels of estradiol and corticosterone in rats. Thereafter, IF results suggested that OVX dramatically induced the increasing of the number of activated microglial cells in prefrontal cortices and the level of M1-type marker iNOS. Finally, PCR results demonstrated that, compared with the sham group, the proinflammatory and prooxidative genes, such as IL-1β, IL-6, TNF-α, iNOS, and CX3CR1, were upregulated in the prefrontal cortices of OVX rats after CUS stimulation, whereas the anti-inflammatory factor Arg1 and microglial cell negative regulatory factor CD200 were downregulated. To sum up, OVX enhances the CUS-mediated anxiety and depression phenomena in rats, and its mechanism may be related to inducing the activation and polarization of microglial cells in the prefrontal cortex of animal and to accelerating the inflammatory response.


Chemosphere ◽  
2011 ◽  
Vol 82 (11) ◽  
pp. 1589-1596 ◽  
Author(s):  
Hongyan Li ◽  
Ming Han ◽  
Lin Guo ◽  
Guangke Li ◽  
Nan Sang

2008 ◽  
Vol 93 (8) ◽  
pp. 3226-3229 ◽  
Author(s):  
Alessandra Bosutti ◽  
Grazia Malaponte ◽  
Michela Zanetti ◽  
Pietro Castellino ◽  
Martina Heer ◽  
...  

Abstract Context: Energy balance and physical activity potentially influence systemic inflammation. Objective: Our objective was to test the hypothesis that moderate energy restriction may prevent activation of inactivity-induced inflammatory response. Design: Participants were studied four times at the end of 14-d periods of experimental bed rest or controlled ambulation, after receiving eucaloric or hypocaloric diets. Setting: The study was conducted at the clinical research center of the German Space Agency. Subjects: Nine healthy young volunteers participated. Interventions: Energy intake was calibrated to physical activity and decreased by about 20% in hypocaloric conditions. Main Outcome Measures: Changes in body fat by dual-energy x-ray absorptiometry as well as plasma inflammatory markers and cytokine mRNA levels in blood cells were measured. Results: Fat mass did not change significantly in eucaloric conditions and decreased in hypocaloric periods (−1.0 ± 0.3 and −1.0 ± 0.3 kg in ambulatory and bed rest, respectively). Bed rest in eucaloric conditions increased plasma C-reactive protein (CRP) (+143 ± 53%) and both the ratios between plasma IL-6 and IL-10 (4±1 times) and white blood cell IL-6 and IL-10 mRNAs (5 ± 1 times). Energy restriction prevented bed-rest-mediated increases in CRP and the IL-6 to IL-10 ratio. Bed rest increased (P = 0.03) long pentraxin-3 (PTX3) plasma concentration, without significant activity-by-diet interaction. In all conditions (n = 36), CRP and PTX3 were inversely correlated (r = −0.61; P &lt; 0.001). Changes in fat mass, leptin, and IL-6 directly correlated with CRP and inversely correlated with PTX3. IL-10 inversely correlated with CRP and directly correlated with PTX3 (r = 0.52; P &lt; 0.01). Conclusions: Calorie restriction prevents the inflammatory response induced by 14 d of bed rest. We suggest an inverse regulation of CRP and PTX3 in response to changes in energy balance.


Author(s):  
Mark Harrison

This chapter describes the pathology of inflammatory response as it applies to Emergency Medicine, and in particular the Primary FRCEM examination. The chapter outlines the key details of normal vs abnormal response, and inflammatory markers including C-reactive protein, rheumatoid factor, and antinuclear factor. This chapter is laid out exactly following the RCEM syllabus, to allow easy reference and consolidation of learning.


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