Maternal antibiotic use and child asthma: is the association causal?

Zhang, Mingyu; Litonjua, Augusto A.; Mueller, Noel T.

doi:10.1183/13993003.01007-2018

Cited by 9 publications

(14 citation statements)

References 37 publications

(38 reference statements)

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“…Another plausible explanation is the observation that allergic conditions likely start at an early age in developing countries, as a result of frequent and early use of antibiotics in children for various infections. 24 In the present study, the first symptoms and the diagnosis of UCAR in most patients occurred at or below 10 years of age. The reason for this coincidence is not clear.…”

Section: Ucar and Agesupporting

confidence: 46%

“…The three medical institutions where the study was carried out may have been targeted by parents because they each have an attending ENT specialist. Another plausible explanation is the observation that allergic conditions likely start at an early age in developing countries, as a result of frequent and early use of antibiotics in children for various infections …”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Pattern of uncontrolled allergic rhinitis in a hospital setting of Kinshasa, Democratic Republic of Congo

Kakobo

Kalala

Kelekele

et al. 2019

Immunity Inflam & Disease

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AimTo determine the clinical and allergic features of uncontrolled allergic rhinitis (UCAR) in the Democratic Republic of Congo (DRC).MethodsObservational cross‐sectional study of 311 patients with UCAR. Allergic rhinitis was diagnosed clinically with sensitization to inhalant allergens and then confirmed by skin prick test. Severity was assessed using the Visual Analog Scale (VAS), with VAS scores greater than or equal to 5 used as cut off to determine uncontrolled status.ResultsThe mean age of UCAR patients was 30.7 ± 15.1 years and 66.9% of the patients were females. Three out of four patients had persistent UCAR while the remainder had intermittent symptoms. UCAR was associated with rhinosinusitis and asthma in 18.6% and 18% of the patients, respectively. Among UCAR patients, 95.2% were polysensitized. The allergens most frequently involved were mites (82%), cat (27.3%), and dog (26.7%). The most frequent symptoms were nasal congestion, sneezing, and runny nose. There were 44.4% of the patients treated with nasal corticosteroids and 33.1% with oral antihistamine (anti‐H1).ConclusionsThis study reports on the clinical phenotype of UCAR in the DRC. The findings contribute to our understanding of UCAR in this population and may be used to implement strategies to reduce the prevalence and burden of UCAR in this setting.

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Section: Ucar and Agesupporting

confidence: 46%

Section: Discussionmentioning

confidence: 99%

Pattern of uncontrolled allergic rhinitis in a hospital setting of Kinshasa, Democratic Republic of Congo

Kakobo

Kalala

Kelekele

et al. 2019

Immunity Inflam & Disease

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“…One compelling target for the prevention of early life obesity is the infant gut microbiome [3]. Prenatal antibiotic exposure has been shown to disturb the colonization and maturation of the infant microbiome [3, 4]. Recently, there has been growing interest in understanding whether prenatal antibiotics alter child growth and adiposity.…”

Section: Introductionmentioning

confidence: 99%

Association of prenatal antibiotics with measures of infant adiposity and the gut microbiome

Zhang

Differding

Benjamin‐Neelon

et al. 2019

Ann Clin Microbiol Antimicrob

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Background Prenatal antibiotic exposure has been associated with an altered infant gut microbiome composition and higher risk of childhood obesity, but no studies have examined if prenatal antibiotics simultaneously alter the gut microbiome and adiposity in infants. Method In this prospective study (Nurture: recruitment 2013–2015 in North Carolina, United States), we examined in 454 infants the association of prenatal antibiotic exposure (by any prenatal antibiotic exposure; by trimester of pregnancy; by number of courses; by type of antibiotics) with infant age- and sex-specific weight-for-length z score (WFL-z) and skinfold thicknesses (subscapular, triceps, abdominal) at 12 months of age. In a subsample, we also examined whether prenatal antibiotic exposure was associated with alterations in the infant gut microbiome at ages 3 and 12 months. Results Compared to infants not exposed to prenatal antibiotics, infants who were exposed to any prenatal antibiotics had 0.21 (95% confidence interval [CI] 0.02, 0.41) higher WFL-z at 12 months, and 0.28 (95% CI 0.02, 0.55) higher WFL-z if they were exposed to antibiotics in the second trimester, after adjustment for potential confounders, birth weight, and gestational age. We also observed a dose-dependent association (P-value for trend = 0.006) with infants exposed to ≥ 3 courses having 0.41 (95% CI 0.13, 0.68) higher WFL-z at 12 months. After further adjustment for delivery method, only second-trimester antibiotic exposure remained associated with higher infant WFL-z (0.27, 95% CI 0.003, 0.54) and subscapular skinfold thickness (0.49 mm, 95% CI 0.11, 0.88) at 12 months. Infants exposed to second-trimester antibiotics versus not had differential abundance of 13 bacterial amplicon sequence variants (ASVs) at age 3 months and 17 ASVs at 12 months (false discovery rate adjusted P-value < 0.05). Conclusions Prenatal antibiotic exposure in the second trimester was associated with an altered infant gut microbiome composition at 3 and 12 months and with higher infant WFL-z and subscapular skinfold thickness at 12 months. Electronic supplementary material The online version of this article (10.1186/s12941-019-0318-9) contains supplementary material, which is available to authorized users.

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“…Several reports have indicated that antibiotic use can induce asthma [ 125 , 126 , 127 ]. The use of antibiotics before and after pregnancy reportedly increases the incidence of childhood asthma [ 128 ]. The functions of CD4 + T cells can be altered by antibiotic use, subsequently provoking the development of eosinophilic asthma.…”

Section: Dysbiosis-induced Asthmamentioning

confidence: 99%

The Role of CD4+ T Cells and Microbiota in the Pathogenesis of Asthma

Jeong

Lee

2021

IJMS

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Asthma, a chronic respiratory disease involving variable airflow limitations, exhibits two phenotypes: eosinophilic and neutrophilic. The asthma phenotype must be considered because the prognosis and drug responsiveness of eosinophilic and neutrophilic asthma differ. CD4+ T cells are the main determinant of asthma phenotype. Th2, Th9 and Tfh cells mediate the development of eosinophilic asthma, whereas Th1 and Th17 cells mediate the development of neutrophilic asthma. Elucidating the biological roles of CD4+ T cells is thus essential for developing effective asthma treatments and predicting a patient’s prognosis. Commensal bacteria also play a key role in the pathogenesis of asthma. Beneficial bacteria within the host act to suppress asthma, whereas harmful bacteria exacerbate asthma. Recent literature indicates that imbalances between beneficial and harmful bacteria affect the differentiation of CD4+ T cells, leading to the development of asthma. Correcting bacterial imbalances using probiotics reportedly improves asthma symptoms. In this review, we investigate the effects of crosstalk between the microbiota and CD4+ T cells on the development of asthma.

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Maternal antibiotic use and child asthma: is the association causal?

Abstract: @ERSpublicationsMaternal antibiotic use before, during and after pregnancy is associated with higher child asthma risk. Lack of specificity to the pregnancy period suggests the association is not causal or the window of susceptibility extends outside pregnancy.

Cited by 9 publications

References 37 publications

Pattern of uncontrolled allergic rhinitis in a hospital setting of Kinshasa, Democratic Republic of Congo

Pattern of uncontrolled allergic rhinitis in a hospital setting of Kinshasa, Democratic Republic of Congo

Association of prenatal antibiotics with measures of infant adiposity and the gut microbiome

The Role of CD4+ T Cells and Microbiota in the Pathogenesis of Asthma

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