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Infection Blocks Lung's Protective Response Against Tobacco Smoke 

An infection that often goes undetected can block the lung's natural protective response against tobacco smoke, according to researchers at National Jewish Health. The findings, recently published online and scheduled to appear in the October issue of Infection and Immunity, suggest one mechanism that may cause smokers to develop chronic obstructive pulmonary disease.

"Although smoking is the overwhelming cause of chronic obstructive pulmonary disease (COPD), only 20 percent of smokers develop the disease," said Brian Day, senior author on the study and Professor of Medicine at National Jewish Health. "Our findings suggest that Mycoplasma pneumoniae (Mp) infection may be one of the co-factors that lead to COPD and other diseases among smokers."

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• Infection blocks lung's protective response against tobacco smoke 

An infection that often goes undetected can block the lung's natural protective response against tobacco smoke, according to researchers at National Jewish Health. The findings, recently published online and scheduled to appear in the October issue of Infection and Immunity, suggest one mechanism that may cause smokers to develop chronic obstructive pulmonary disease.

"Although smoking is the overwhelming cause of chronic obstructive pulmonary disease (COPD), only 20 percent of smokers develop the disease," said Brian Day, senior author on the study and Professor of Medicine at National Jewish Health. "Our findings suggest that Mycoplasma pneumoniae (Mp) infection may be one of the co-factors that lead to COPD and other diseases among smokers." . . .

It has long been known that the lungs mount a strong protective response against tobacco smoke, which the National Jewish researchers confirmed in their studies in mice and cell cultures. They found that mice exposed to tobacco smoke for 16 weeks doubled the amount of the antioxidant glutathione in the fluid bathing the airways. The antioxidant reacts with the reactive species in tobacco smoke, thus preventing damaging reactions with lung tissue.

"This natural protective response actually allows people to smoke," said Day. "Without it, all smokers would suffer significantly more lung damage."

Previous work in Dr. Day's lab had suggested that lung infections might affect the lung's protective response.

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Cigarette smoke worsens lung inflammation and impairs resolution of influenza infection in mice 

Cigarette smoke has both pro- inflammatory and immunosuppressive effects. Both active and passive cigarette smoke exposure are linked to an increased incidence and severity of respiratory virus infections, but underlying mechanisms are not well defined.

We hypothesized, based on prior gene expression profiling studies, that upregulation of pro-inflammatory mediators by short term smoke exposure would be protective against a subsequent influenza infection. . . .

Conclusion: Smoke induced inflammation does not protect against influenza infection. In most respects, smoke exposure worsened the host response to influenza.

This animal model may be useful in studying how smoke worsens respiratory viral infections.

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Yale study shows why cigarette smoke makes flu, other viral infections worse 

A new study by researchers at Yale School of Medicine could explain why the cold and flu virus symptoms that are often mild and transient in non-smokers can seriously sicken smokers. Published in the Journal of Clinical Investigation, the study also identified the mechanism by which viruses and cigarette smoke interact to increase lung inflammation and damage.

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Cigarette smoke and sick people don't mix ($$) 

People who are exposed to cigarette smoke when they're sick might be making themselves feel worse.

Researchers at Yale University found the combination of viral cells and cigarette smoke caused more severe airway damage, and worsened flu symptoms in mice.

They also identified how the enhancement of cold symptoms happens when people smoke, they hope to use this information in future studies.

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Smoking Conspires with Viruses to Advance COPD 

NEW HAVEN, Conn., July 24 -- Cigarette smoke in mice can exaggerate lung responses to viral infections, which could explain some heretofore mysterious aspects of chronic obstructive pulmonary disease, researchers here said

Mice infected with influenza virus showed higher lung levels of cytokines and other inflammatory markers and more extensive alveolar remodeling when they breathed cigarette smoke rather than plain room air, reported Jack A. Elias, M.D., of Yale, and colleagues online in the Journal of Clinical Investigation.

Both smoke and viral infection were required to see the alveolar remodeling, they found. Uninfected animals showed no difference in alveolar chord length if they breathed smoke versus room air.

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How irritating: the role of TRPA1 in sensing cigarette smoke and aerogenic oxidants in the airways 

Airway irritants cause a variety of lung pathologies. Two separate studies, the first recently reported in the JCI by Bessac et al. and the second reported by Andrè et al. in the current issue of the JCI (see the related article beginning on page 2574), have identified irritants that activate transient receptor potential cation channel, subfamily A, member 1 (TRPA1) receptors in airway sensory neurons, resulting in neurogenic inflammation and respiratory hypersensitivity. The identification of TRPA1 activation by toxicants from cigarette smoke and polluted air, such as crotonaldehyde, acrolein, and oxidizing agents such as hydrogen peroxide, is an important finding. These two studies enhance our understanding of how pollution and cigarette smoke can damage airway function and will hopefully pave the way for the development of rational alternative therapeutics for such airway injury.

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Cigarette smoke–induced neurogenic inflammation is mediated by α,β-unsaturated aldehydes and the TRPA1 receptor in rodents 

Cigarette smoke (CS) inhalation causes an early inflammatory response in rodent airways by stimulating capsaicin-sensitive sensory neurons that express transient receptor potential cation channel, subfamily V, member 1 (TRPV1) through an unknown mechanism that does not involve TRPV1. We hypothesized that 2 α,β-unsaturated aldehydes present in CS, crotonaldehyde and acrolein, induce neurogenic inflammation by stimulating TRPA1, an excitatory ion channel coexpressed with TRPV1 on capsaicin-sensitive nociceptors. We found that CS aqueous extract (CSE), crotonaldehyde, and acrolein mobilized Ca2+ in cultured guinea pig jugular ganglia neurons and promoted contraction of isolated guinea pig bronchi. These responses were abolished by a TRPA1-selective antagonist and by the aldehyde scavenger glutathione but not by the TRPV1 antagonist capsazepine or by ROS scavengers. Treatment with CSE or aldehydes increased Ca2+ influx in TRPA1-transfected cells, but not in control HEK293 cells, and promoted neuropeptide release from isolated guinea pig airway tissue. Furthermore, the effect of CSE and aldehydes on Ca2+ influx in dorsal root ganglion neurons was abolished in TRPA1-deficient mice. These data identify α,β-unsaturated aldehydes as the main causative agents in CS that via TRPA1 stimulation mediate airway neurogenic inflammation and suggest a role for TRPA1 in the pathogenesis of CS-induced diseases.

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How cigarette smoke negatively impacts the consequences of viral infections 

Jack Elias and colleagues, at Yale University School of Medicine, have performed new studies in mice that provide mechanistic insight into why viral infections have more severe consequences in individuals exposed to cigarette smoke than in those not exposed to cigarette smoke (e.g., influenza-infected smokers have increased mortality when compared with influenza-infected nonsmokers).

In the study, a combination of cigarette smoke and compounds that mimic viral components were found to cause more severe airway damage in a mouse model of the lung disease chronic obstructive pulmonary disease than the compounds that mimic viral components alone. Further, cigarette smoke enhanced the effects of influenza in mice.

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• Smokers Struck by Influenza Face Higher Mortality Rates  

In experiments with mice, U.S. researchers have discovered why viral infections have more severe consequences in smokers than in nonsmokers. For example, smokers with influenza are more likely to die than nonsmokers with influenza.

The Yale University School of Medicine team found that a combination of cigarette smoke and compounds that mimic viral components caused more severe airway damage in a mouse model of chronic obstructive pulmonary disease (COPD) than the compounds that mimic viral components alone.

In addition, cigarette smoke further enhanced the effects of influenza in mice, the study found. . . .

The study was published in the current issue of the Journal of Clinical Investigation.

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• Technology uses tobacco plants to fight cancer  

A personalized vaccine made using tobacco plants -- normally associated with causing cancer rather than helping cure it -- could aid people with lymphoma in fighting the disease, U.S. researchers said on Monday.

The treatment, which would vaccinate cancer patients against their own tumor cells, is made using a new approach that turns genetically engineered tobacco plants into personalized vaccine factories.

"This is the first time a plant has been used for making a protein to inject into a person," said Dr. Ron Levy of Stanford University School of Medicine in California, whose research appears in the journal Proceedings of the National Academy of Sciences.

"This would be a way to treat cancer without side effects," Levy said in a statement. "The idea is to marshal the body's own immune system to fight cancer."

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Cigarette smoke worsens lung inflammation and impairs resolution of influenza infection in mice 

Conclusion

Smoke induced inflammation does not protect against influenza infection. In most respects, smoke exposure worsened the host response to influenza. This animal model may be useful in studying how smoke worsens respiratory viral infections.

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Diagnosis of Chronic Obstructive Pulmonary Disease  

Chronic obstructive pulmonary disease affects more than 26 million adults in the United States. Family physicians provide care for most of these patients. Cigarette smoking is the leading risk factor for chronic obstructive pulmonary disease, although other risk factors, including occupational and environmental exposures, account for up to one in six cases. Patients presenting with chronic cough, increased sputum production, or progressive dyspnea should be evaluated for the disease. Asthma is the disease most often confused with chronic obstructive pulmonary disease. The diagnosis of chronic obstructive pulmonary disease is based on clinical suspicion and spirometry confirmation. A forced expiratory volume in one second/ forced vital capacity ratio that is less than 70 percent, and that is incompletely reversible with the administration of an inhaled bronchodilator, suggests chronic obstructive pulmonary disease. . . .

COPD is defined as an inflammatory respiratory disease, largely caused by exposure to tobacco smoke. . . .

Cigarette smoking is the primary risk factor for COPD. More than 80 percent of deaths from the disease are directly attributable to smoking, and persons who smoke are 12 to 13 times more likely to die from COPD than nonsmokers. 6 the absolute risk of COPD among active, continuous smokers is at least 25 percent.7

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Early smoke exposure ups serious infection risk 

Children who are exposed to secondhand tobacco smoke early in life are at greater risk of being hospitalized for infections than those brought up in a smoke-free environment, researchers from Hong Kong report.

The risk of being hospitalized was greatest among babies 6 months old and younger, but the increased risk persisted up until the children were 8 years old, Dr. M. K. Kwok of the University of Hong Kong and colleagues found. Children who were premature or low birth weight were particularly vulnerable.

The findings suggest that secondhand smoke exposure may not only be harmful to children's respiratory tracts, but to their immune systems as well, Kwok and colleagues say.

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• Smoking and human papillomavirus infection: pooled analysis of the International Agency for Research on Cancer HPV Prevalence Surveys  

Background

Smoking increases the risk of squamous-cell carcinoma of the cervix, but it is not clear whether smoking increases the risk of acquisition or persistence of human papillomavirus (HPV) infection.

Methods

Information on smoking was collected from 10 areas in four continents among population-based, age-stratified random samples of women aged 15 years or older. . . .

Conclusions

Our study suggests that current, though not former, smoking is associated with an increased prevalence of HPV, after allowance for sexual covariates. Among current smokers, HPV prevalence increased with smoking intensity, but a clear dose–response relationship was exclusively seen among women who declared one lifetime sexual partner.

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