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One of the most pressing issues in global health is air pollution. Emissions from traffic-related air pollution and biomass burning are two of the most common sources of air pollution. Diesel exhaust (DE) and wood smoke (WS) have been used as models of these pollutant sources in controlled human exposure (CHE) experiments. The aim of this review was to compare the health effects of DE and WS using results obtained from CHE studies. A total of 119 CHE-DE publications and 25 CHE-WS publications were identified for review. CHE studies of DE generally involved shorter exposure durations and lower particulate matter concentrations, and demonstrated more potent dysfunctional outcomes than CHE studies of WS. In the airways, DE induces neutrophilic inflammation and increases airway hyperresponsiveness, but the effects of WS are unclear. There is strong evidence that DE provokes systemic oxidative stress and inflammation, but less evidence exists for WS. Exposure to DE was more prothrombotic than WS. DE generally increased cardiovascular dysfunction, but limited evidence is available for WS. Substantial heterogeneity in experimental methodology limited the comparison between studies. In many areas, outcomes of WS exposures tended to trend in similar directions to those of DE, suggesting that the effects of DE exposure may be useful for inferring possible responses to WS. However, several gaps in the literature were identified, predominantly pertaining to elucidating the effects of WS exposure. Future studies should strongly consider performing head-to-head comparisons between DE and WS using a CHE design to determine the differential effects of these exposures.
One of the most pressing issues in global health is air pollution. Emissions from traffic-related air pollution and biomass burning are two of the most common sources of air pollution. Diesel exhaust (DE) and wood smoke (WS) have been used as models of these pollutant sources in controlled human exposure (CHE) experiments. The aim of this review was to compare the health effects of DE and WS using results obtained from CHE studies. A total of 119 CHE-DE publications and 25 CHE-WS publications were identified for review. CHE studies of DE generally involved shorter exposure durations and lower particulate matter concentrations, and demonstrated more potent dysfunctional outcomes than CHE studies of WS. In the airways, DE induces neutrophilic inflammation and increases airway hyperresponsiveness, but the effects of WS are unclear. There is strong evidence that DE provokes systemic oxidative stress and inflammation, but less evidence exists for WS. Exposure to DE was more prothrombotic than WS. DE generally increased cardiovascular dysfunction, but limited evidence is available for WS. Substantial heterogeneity in experimental methodology limited the comparison between studies. In many areas, outcomes of WS exposures tended to trend in similar directions to those of DE, suggesting that the effects of DE exposure may be useful for inferring possible responses to WS. However, several gaps in the literature were identified, predominantly pertaining to elucidating the effects of WS exposure. Future studies should strongly consider performing head-to-head comparisons between DE and WS using a CHE design to determine the differential effects of these exposures.
Colorectal cancer (CRC) is one of the most common malignancies in the world, with a global incidence of almost 2 million new cases every year. Despite the availability of many diagnostic tests, including laboratory tests and molecular diagnostics, an increasing number of new cases is observed. Thus, it is very important to search new markers that would show high diagnostic sensitivity and specificity in the detection of colorectal cancer in early stages of the disease. Eotaxins are proteins that belong to the cytokine group—small molecules with a variety of applications. Their main role is the activation of basophils and eosinophils involved in inflammatory processes. Therefore, we performed an extensive search of the literature pertaining to our investigation via the MEDLINE/PubMed database. On the basis of available literature, we can assume that eotaxins accumulate in cancer cells in the course of CRC. This leads to a decrease in the chemotaxis of eosinophils, which are effector immune cells with anti-tumor activity. This may explain a decrease in their number as a defense mechanism of cancer cells against their destruction and may be useful when attempting anti-tumor therapy with the use of chemokines.
Asthma is a chronic inflammatory disease related to the immune response of type 2 T helper cells (Th2), which affects all age groups. The incidence of asthma is increasing worldwide, and it has become a significant public health problem. This study aimed to investigate the immunomodulatory effects of Lacticaseibacillus (formerly Lactobacillus) paracasei K47 on mice with ovalbumin (OVA)-induced allergy. The consequences of orally administered heat-inactivated K47 in OVA-sensitised/challenged BALB/c mice were evaluated by assessing the serum levels of immunoglobulins (Igs), airway hyperresponsiveness (AHR), and bronchoalveolar lavage fluid (BALF) cytokine. In addition, the effect of K47 on type 1 T helper cells (Th1)/Th2 cytokine production in splenocytes from OVA-sensitised mice was evaluated. The results revealed that supplementation with K47 remarkably reduced serum levels of total IgE, OVA-specific IgE, and OVA-specific IgG1 in OVA-sensitised/challenged mice. In addition, K47 intervention ameliorated AHR and suppressed the accumulation of inflammatory cells in the BALF of OVA-sensitised/challenged mice. Furthermore, the immunomodulatory ability of K47 was mediated by regulation of the cytokine profile toward the Th1 response in the BALF, and splenocytes of OVA-sensitised mice. Taken together, these results suggested that K47 can modulate the host immune response to ameliorate AHR and inflammation in allergic asthma.
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