1918: Defence of the Respiratory Membrane Against Influenza, etc

[mixin]

A poison gas like ozone, phosagene, or chlorine, when inhaled is concentrated by solution in the secretion covering the membrane, and the membrane defends itself by secreting fluid and so diluting and washing away the poison..
The membrane responds in the same way to bacterial toxins.

There is some evidence (this is now being investigated) that workers in S02 factories are relatively free from colds, also those in commercial gas works; chemical manufacters, as a class, have a low phthisis mortality rate; the taking of ordinary snuff has been praised for keeping off influenza; nose-drill and the daily use of some mild antiseptic as a nasal wash, snuff, or spray arerecommended for the same purpose; and recently evidence has come forth of considerable interest-namely, that the clerks in certain offices of the electric tube railways ventilated witlh ozone-air had 3% of absences in the late epidemic, while the clerks in the other offlces, not so ventilated, had 10%.

All these agencies, just as the antiseptics used by surgeons in wound and Almroth Wright's salt treatment, have the effect of drawing out lymph, and so washing and cleansing the part. In the case of the respiratory membrane they take the place of the natural action of breathing the cool outside air. The smelling salts which used to be popular must play the same part.

(Here was discussion about the gas workers http://www.flutrackers.com/forum/showthread.php?t=86467)

...I have put forward the important influence which cool air -cool and therefore of low vapour tension- has on bringing more arterial blood to the respiratory membrane and increasing evaporation from and therefore flow of tissue lymph through it. Warm moist atmospheres are against this natural washing and immunizing defence. In this, I claim, lies one explanation of the good effect of open air treatmaent, and the ill effect of crowded tenements.
Exercise in the open air, by increasing the breathing perhaps five times, greatly increases the blood flow through and evaporation from the respiratory membrane, and in this lies one of the good effects of exercise.

I find the cooling, and therefore the evaporative, power of the air is by no means spent in the nose, but acts on the deeper parts and probably right down to the smaller tubes of the lung. Especially is this the case when the breathing is made deep and the lungs fully expanded. A person may in an hour easily evaporate an ounce and a half of water from his membrane when taking exercise in cold weather.

There, is another thing to consider, namely, the actual cooling of the membrane, which may check the growth of sensitive pathogenic bacteria-for example, those of cerebrospinal fever. Mouth breatling, or a blocked airway on one side of the nose, keeps the nose (or one side of it) at a higher temperature, and makes it a better incubator for the growth of such bacteria, while it lessens blood flow through and evaporation from it.

To combat the influenza infection, then, I would urge the deep breathing of cool air, brought about by exercise, sleeping in open air, and as an adjunct any spray, gargle, or snuff wlhich enhances the outflow of secretion from the respiratory membrane of the nose and throat.

(Included are a lot of experiments he did which show breathing in through the nose and exhaling through the mouth cools the nose best. )

A difference is clear, without carrying through the full calculation, between- the frosty open air and this very cold room. It is very great between cold and warm humid air, and the sudden change from one to the other obviouslystrains the functions of the membrane. The body is protected by clothes-not so the respiratory membrane. Hence the need to stay in a uniform atmosphere when infected with a catarrh.
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2340872&blobtype=pdf

 

[gsgs]

Re: 1918: Defence of the Respiratory Membrane Against Influenza, etc

this is whisdom from 1919.
We can assume that this all had been examined more
extensively in the meantime and that practical
uses didn't come out of it.
Else they would have told us (?!?)

 

[mixin]

Re: 1918: Defence of the Respiratory Membrane Against Influenza, etc

Well, we sometimes find that old wisdom still works; it's just often forgotten.

My grandmother always made me gargle with saltwater for colds, etc, which they still recommend today. Nasal lavage is still being done. I wonder if people who sleep with their bedroom windows open in cold weather have less respiratory infections?

His opinion on deep breathing is likely good, unless a person was being exposed to flu viruses. Then, possibly, a person might not want to inhale deeply into the lungs; maybe shallow breathing might be better? I wonder if the method of breathing makes it easier to catch respiratory diseases?

I'm curious about his theory that lower nose temperature inhibits bacterial growth.

Then, there is the powerful influence of drug companies. They make a lot of money treating symptoms.

 

[gsgs]

Re: 1918: Defence of the Respiratory Membrane Against Influenza, etc

Studies of an influenza A virus temperature sensitive mutant identify a 'late' role for NP in the formation of infectious virions.
temperature sensitive (ts) NP mutant (US3) M239L originally generated in A/chicken/Rostock/34
A/PR/8/34+M239L produced a ts phenotype
profound incompatibility between M239L and the A/Udorn/72 M1 gene

http://www.ncbi.nlm.nih.gov/pubmed/...nel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum



Influenza nose temperature

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39:
Production and level of genetic stability of an influenza A virus temperature-sensitive mutant containing two genes with ts mutations.
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40:
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41:
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Prospects of a living attenuated vaccine against influenza.
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45:
Genetic approaches to attenuation of influenza A viruses for man.
Murphy BR, Markoff LJ, Chanock RM, Spring SB, Maassab HF, Kendal AP, Cox NJ, Levine MM, Douglas RG Jr, Betts RF, Couch RB, Cate TR Jr.
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46:
Growth of influenza A viruses in hamsters.
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47:
Sensitivity to pyrexial temperatures: a factor contributing to virulence differences between two clones of influenza virus.
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Temperature-sensitive mutants of influenza virus. XVI. Transfer of the two ts lesions present in the Udorn/72-ts-1A2 donor virus to the Victoria/3/75 wild-type virus.
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49:
Temperature-sensitive mutants of influenza virus. XV. The genetic and biological characterization of a recombinant influenza virus containing two ts lesions produced by mating two complementing, single lesion ts mutants.
Murphy BR, Wood FT, Massicot JG, Spring SB, Chanock RM.
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50:
Studies with live attenuated influenza vaccines.
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Demonstration of a non-temperature-sensitive growth-restricting mutation in a ts mutant of influenza A virus: implications for live virus vaccine development.
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52:
Thermal stability and interaction with ferret inflammatory exudates of two clones of influenza virus of differing virulence for both ferrets and man.
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53:
Formation of secretory and circulating antibodies after immunization with live and inactivated influenza virus vaccines.
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54:
Differential response of ferrets to infection with virulent and avirulent influenza viruses: a possible marker of virus attenuation.
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55:
Cold adapted variants of influenza A. II. Comparison of the genetic and biological properties of ts mutants and recombinants of the cold adapted A/AA/6/60 strain.
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56:
The behaviour in ferrets of two closely related clones of influenza virus of differing virulence for man.
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57:
Pathogenicity, immunogenicity and genetic stability in mice and ferrets of a cold inhibitor-resistant mutant of influenza H3N2 virus.
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58:
Temperature sensitive mutants of influenza virus. IX. Genetic and biological characterization of TS-1[E] lesions when transferred to a 1972 (H3N2) influenza A virus.
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59:
Temperature-sensitive mutants of influenza. VIII. Genetic and biological characterization of TS mutants of influenza virus A (H3N2) and their assignment to complementation groups.
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60:
Failure of attenuated temperature-sensitive influenza A (H3N2) virus to induce heterologous interference in humans to parainfluenza type 1 virus.
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The protection of ferrets against influenza by immunization with a split influenza vaccine.
Brady MI, Furminger IG.
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New approaches to the control of influenza.
Dowdle WR.
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63:
Immunity to influenza in ferrets. VI. Immunization with adjuvanted vaccines.
Potter CW, Jennings R, McLaren C.
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64:
Immunity to influenza in ferrets. I. Response to live and killed virus.
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65:
Studies of the basis of localization of influenza virus in ferret organ cultures.
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66:
[Interferon production in healthy children and in those ill with acute respiratory and enterovirus infections. 2. Interferon production in patients with acute respiratory infections and its correlation with leukocyte interferon production]
Solov'ev VD, Vorotyntsefa NV, Bektemirov TA, Kleĭmenova ZN, Fedorova IuB.
Vopr Virusol. 1969 May-Jun;14(3):267-70. Russian. No abstract available.
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67:
Immunocytologic and serologic diagnosis of influenza A2.
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