Objectives: The objective of this study was to investigate the prevalence of Mycoplasma pneumoniae and Chlamydophila pneumoniae infections in patients with community-acquired pneumonia (CAP) admitted ...to Beheshti hospital in Kashan.Methods: A descriptive cross-sectional study was conducted on 160 CAP patients admitted to Beheshti hospital in Kashan. Serological tests were performed using the ELISA method to evaluate IgG and IgM antibodies for Mycoplasma and Chlamydia pneumoniae. A questionnaire was also completed, which included demographic data, hospitalization time, and clinical and paraclinical findings. The data were analyzed using SPSS software (version 20).Results: The study found that 19 (11.9%) cases tested positive for M. pneumoniae IgM antibodies, while 132 (82.5%) cases tested positive for M. pneumoniae IgG antibodies. For C. pneumoniae, 16 (10%) cases tested positive for IgM antibodies, and 151 (94.4%) cases tested positive for IgG antibodies. There was no significant association between M. pneumoniae and Chlamydia pneumoniae infections with sex, underlying illness, pneumonia severity, ICU admission, hospital death, hospitalization time, CRP, hematocrit, and platelet count. However, a significant relationship was observed between M. pneumoniae and chief complaint (p<0.001), as well as age (p = 0.122). Additionally, a significant relationship was found between C. pneumoniae and white blood cell count (p = 0.001), as well as changes in chest radiography (p = 0.001).Conclusion: Given the significant incidence of atypical infections in CAP patients and the difficulties in laboratory detection, effective antibiotics targeting Mycoplasma pneumoniae and Chlamydophila pneumoniae are strongly suggested in the empirical therapy of CAP.
Infections have been linked to the development of cardiovascular disease and atherosclerosis. Findings from the past decade have identified microbial ecosystems residing in different habitats of the ...human body that contribute to metabolic and cardiovascular-related disorders. In this Review, we describe three pathways by which microbiota might affect atherogenesis. First, local or distant infections might cause a harmful inflammatory response that aggravates plaque development or triggers plaque rupture. Second, metabolism of cholesterol and lipids by gut microbiota can affect the development of atherosclerotic plaques. Third, diet and specific components that are metabolized by gut microbiota can have various effects on atherosclerosis; for example, dietary fibre is beneficial, whereas the bacterial metabolite trimethylamine-N-oxide is considered harmful. Although specific bacterial taxa have been associated with atherosclerosis, which is supported by increasing mechanistic evidence, several questions remain to be answered to understand fully how the microbiota contributes to atherosclerosis and cardiovascular disease. Such knowledge might pave the way for novel diagnostics and therapeutics based on microbiota.
This article reviews research results and ideas presented at a special symposium at the International Association of Gerontology and Geriatrics (IAGG) Congress held in July 2017 in San Francisco. ...Five researchers presented their results related to infection and Alzheimer's disease (AD). Prof. Itzhaki presented her work on the role of viruses, specifically HSV-1, in the pathogenesis of AD. She maintains that although it is true that most people harbor HSV-1 infection, either latent or active, nonetheless aspects of herpes infection can play a role in the pathogenesis of AD, based on extensive experimental evidence from AD brains and infected cell cultures. Dr. Miklossy presented research on the high prevalence of bacterial infections that correlate with AD, specifically spirochete infections, which have been known for a century to be a significant cause of dementia (e.g., in syphilis). She demonstrated how spirochetes drive senile plaque formation, which are in fact biofilms. Prof. Balin then described the involvement of brain tissue infection by the
bacterium, with its potential to use the innate immune system in its spread, and its initiation of tissue damage characteristic of AD. Prof. Fülöp described the role of AD-associated amyloid beta (Aβ) peptide as an antibacterial, antifungal and antiviral innate immune effector produced in reaction to microorganisms that attack the brain. Prof. Barron put forward the novel hypothesis that, according to her experiments, there is strong sequence-specific binding between the AD-associated Aβ and another ubiquitous and important human innate immune effector, the cathelicidin peptide LL-37. Given this binding, LL-37 expression in the brain will decrease Aβ deposition via formation of non-toxic, soluble Aβ/LL-37 complexes. Therefore, a chronic underexpression of LL-37 could be the factor that simultaneously permits chronic infections in brain tissue and allows for pathological accumulation of Aβ. This first-of-its-kind symposium opened the way for a paradigm shift in studying the pathogenesis of AD, from the "amyloid cascade hypothesis," which so far has been quite unsuccessful, to a new "infection hypothesis," or perhaps more broadly, "innate immune system dysregulation hypothesis," which may well permit and lead to the discovery of new treatments for AD patients.
Previous studies have tended to relate Chlamydia pneumoniae (Cpn) infection to atherosclerosis. However, while serological studies have mostly reinforced this hypothesis, inconsistent and even ...contradictory findings have been reported in various researches. Recent papers have pointed to the significance of Cpn in atherosclerotic lesions, which are regarded as the initiator and cause of chronic inflammation. This bacterium develops atherosclerosis by phenotypic changes in vascular smooth muscle cells, dysregulation of endothelin-1 in the vascular wall, and releasing pro-inflammatory cytokines from Toll-like receptor-2 (TLR2). Furthermore, Cpn infection, particularly under hyperlipidemic conditions, enhances monocyte adhesion to endothelium; changes the physiology of the host, e.g., cholesterol homeostasis; and activates the Low-density lipoprotein (LDL) receptor, which is the initial step in atherogenesis. On the other hand, it has been reported that Cpn, even without the immune system of the host, has the ability to stimulate arterial thickening. Moreover, there is evidence that Cpn can increase the impact of the classical risk factors such as hyperlipidemia, pro-inflammatory cytokines, and smoking for atherosclerosis. Furthermore, animal studies have shown that Cpn infection can induce atherosclerotic, which alongside hyperlipidemia is a co-risk factor for cardiovascular disease. Although the exact link between Cpn and atherosclerosis has not been determined yet, previous studies have reported possible mechanisms of pathogenesis for this bacterium. Accordingly, investigating the exact role of this infection in causing atherosclerosis may be helpful in controlling the disease.
•The possible association between Chlamydia pneumoniae (Cpn) and Atherosclerosis has been suggested since the 1990's.•The presence of Cpn in atherosclerotic lesions has been reported using different methods including serology, immunocytochemistry, PCR, and in situ DNA hybridization.•Stronger evidence from in vivo studies performed on animal models and molecular experiments helps clarify the association between Cpn and atherosclerosis.•More studies are needed to determine the exact role of Cpn in the procedure that led to atherosclerosis.
Objective: To determine the prevalence of infection due to atypical microorganisms in cases of communityacquired pneumonia in adult inmunocompetent patients seeking attention in the Hospital Nacional ...Hipolito Unanue. Methods: Adult inmunocompetent patients seeking medical attention in the emergency ward of Hospital Hipolito Unanue with diagnosis of community-acquired pneumonia were evaluated between september 2008 and january 2009. Blood samples were drawn for Mycoplasma pneumoniae and Chlamydia pneumoniae serology, by the detection of M Inmunoglobulin by ELISA technique. Results: We recruited 85 patients. The average age was 65.33 ± 21.43 years. We found 3 cases with positive IgM serology against M. pneumoniae and 1 case positive against C. pneumoniae. The antibody titers against M. pneumoniae had a highly significant correlation with the age (r=-0.28; p<0.01). We also found a statistically significant difference between the titers of antibodies against M. pneumoniae and those correspondent to C. pneumoniae (r=0.29; p<0.01). Conclusion: Infection due to atypical microorganisms doesn’t seem to be a frequent condition in inpatients with diagnosis of community-acquired pneumonia. Research in larger populations, including outpatients should be done, in order to define the role of atypical pathogens in cases of pneumonia at a national level.
Atherosclerotic vascular disease (ASVD) is a chronic process, with a progressive course over many years, but it can cause acute clinical events, including acute coronary syndromes (ACS), myocardial ...infarction (MI) and stroke. In addition to a series of typical risk factors for atherosclerosis, like hyperlipidemia, hypertension, smoking and obesity, emerging evidence suggests that atherosclerosis is a chronic inflammatory disease, suggesting that chronic infection plays an important role in the development of atherosclerosis. Toll-like receptors (TLRs) are the most characteristic members of pattern recognition receptors (PRRs), which play an important role in innate immune mechanism. TLRs play different roles in different stages of infection of atherosclerosis-related pathogens such as
Chlamydia pneumoniae
(
C. pneumoniae
)
,
periodontal pathogens including
Porphyromonas gingivalis
(
P. gingivalis
)
, Helicobacter pylori
(
H. pylori
) and
human immunodeficiency virus
(HIV). Overall, activation of TLR2 and 4 seems to have a profound impact on infection-related atherosclerosis. This article reviews the role of TLRs in the process of atherosclerosis after
C. pneumoniae
and other infections and the current status of treatment, with a view to providing a new direction and potential therapeutic targets for the study of ASVD.
The duration of therapy for community-acquired pneumonia (CAP) remains undefined. We sought to investigate whether short-course antibiotic treatment for CAP is associated with favorable clinical ...outcomes in adult patients. We systematically searched PubMed, EMBASE, the Cochrane Central Register of Controlled Trials, and ClinicalTrials.gov for studies comparing the effectiveness and safety between treatment regimens administered for ≤6 days and ≥7 days. We defined treatment for ≤6 days as short-course treatment and treatment for ≥7 days as long-course treatment. Twenty-one clinical trials (4,861 clinically evaluable patients) were included, and 19 out of 21 trials were randomized. Clinical cure was similar between the compared groups (4,069 patients, risk ratio RR = 0.99 95% confidence interval {CI}, 0.97 to 1.01), irrespective of patient setting (RR = 0.98 95% CI, 0.96 to 1.00 for the outpatient setting and RR = 1.00 95% CI, 0.92 to 1.09 for the inpatient setting) or severity of pneumonia (RR = 1.05 95% CI, 0.96 to 1.14). Also, relapses were similar between the short- and long-course treatment groups (1,923 patients, RR = 0.67 95% CI, 0.30 to 1.46). Short-course treatment was associated with fewer serious adverse events (1,923 patients, RR = 0.73 95% CI, 0.55 to 0.97) and, importantly, resulted in lower mortality than long-course treatment (2,802 patients, RR = 0.52 95% CI, 0.33 to 0.82). In CAP, short-course antibiotic treatment (≤6 days) is as effective as and potentially superior to, in terms of mortality and serious adverse events, longer-course treatment.
The investigation of anti-inflammatory and immunosuppressive functions of Kynurenic acid (KYNA) is now in focus. There is also substantial evidence that TSG-6 has an anti-inflammatory activity. ...Therefore, in the present study, we compared the effects of newly synthetized KYNA analogs on the TNF-α production in U-937 monocytic cells in correlation with the effects on the TSG-6 expression.
TNF-α production was measured by ELISA, the TSG-6 expression was determined by RTqPCR method. As cytokine inducers
and
were used.
KYNA and KYNA analogs attenuated TNF-α production and increased TSG-6 mRNA expression in U-937 cells stimulated by heat inactivated
. In contrast, KYNA and some of the KYNA analogs increased the TNF-α production of
infected U-937 cells; however, the newly synthetized analogs (SZR104, SZR 105, and SZR 109) exerted significant inhibitory effects on the TNF-α synthesis. The inhibitory and stimulatory effects correlated inversely with the TSG-6 expression.
TSG-6 expression following activation with bacterial components could participate in the suppression of inflammatory cytokines, such as TNF-α, We suppose that the elevation of the TSG-6 expression by KYNA and especially by new KYNA analogs might be one of the mechanisms that are responsible for their suppressive effect on TNF-α production as a feedback mechanism. KYNA and KYNA analogs have an important role in influencing TSG-6 expression, and there is a possible benefit of targeting TSG-6 expression by kynurenines in inflammatory conditions following infections.
Chlamydia pneumoniae infection cases have usually accounted for <1.5% of community-acquired respiratory tract infections. Currently, Lausanne, Switzerland is experiencing a notable upsurge in cases, ...with 28 reported within a span of a few months. This upsurge in cases highlights the need for heightened awareness among clinicians.
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