If cavity wall thickness decreases, what does it mean?

Posted by helen1000 @helen1000, Nov 2 11:43pm

I did some research on how antibiotics help change the cavity wall thickness. Does it mean the cavity has a better chance to close if the wall thickness decreases significantly after months' antibiotics treatment? If anyone can share their experience accordingly, that will be much appreciated.

Yes, antibiotics can reduce the thickness of a lung cavity wall and decrease the overall size of the cavity, provided the underlying cause is a treatable bacterial infection, such as a lung abscess or certain pneumonias.
How it Works
Treating the infection: Antibiotics target and eliminate the bacteria causing the infection, which is the primary driver of inflammation and tissue necrosis that forms the cavity and its thick walls.
Reducing inflammation: As the infection resolves, the associated inflammation in the surrounding lung tissue decreases, allowing the cavity walls to become thinner and the lung tissue to heal.
Resolution: In successful cases, the lung abscess or cavitating pneumonia can completely resolve, leaving minimal or no residual scarring, though in some instances a small, thin-walled cyst or some residual fibrosis may remain.

Interested in more discussions like this? Go to the MAC & Bronchiectasis Support Group.

Hope on the Horizon: Signs of Real Lung Regeneration

For years, we’ve been told that once the lungs are damaged by bronchiectasis, that damage can’t be reversed. But a new clinical trial using a patient’s own airway stem cells, called P63⁺ progenitor cells, is challenging that belief in a truly remarkable way.

In this study, patients had a small sample of their own airway cells collected through a bronchoscopy. Those cells were carefully grown and multiplied in the lab, then placed back into the lungs. The hope was that these special cells could help repair damaged tissue and restore lung function. By using autologous airway basal stem cells , it has demonstrated that damaged lung tissue can begin to repair itself. Patients who received these stem cells showed improvements in lung function within months, and imaging studies revealed something remarkable: previously dilated airways were partially shrinking, a clear indication that regeneration of the airway structure is possible. This is the first time we have seen actual structural remodeling in human bronchiectasis lungs, not just slowing of disease or symptom relief.— feeling excited.

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Profile picture for helen1000 @helen1000

Hope on the Horizon: Signs of Real Lung Regeneration

For years, we’ve been told that once the lungs are damaged by bronchiectasis, that damage can’t be reversed. But a new clinical trial using a patient’s own airway stem cells, called P63⁺ progenitor cells, is challenging that belief in a truly remarkable way.

In this study, patients had a small sample of their own airway cells collected through a bronchoscopy. Those cells were carefully grown and multiplied in the lab, then placed back into the lungs. The hope was that these special cells could help repair damaged tissue and restore lung function. By using autologous airway basal stem cells , it has demonstrated that damaged lung tissue can begin to repair itself. Patients who received these stem cells showed improvements in lung function within months, and imaging studies revealed something remarkable: previously dilated airways were partially shrinking, a clear indication that regeneration of the airway structure is possible. This is the first time we have seen actual structural remodeling in human bronchiectasis lungs, not just slowing of disease or symptom relief.— feeling excited.

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@helen1000 Good morning Helen, I see you are in research mode today. I really like your second post, where you cite the article then summarize it.

May I ask where you got the information that you used to start the discussion? Can you cite the source? If it came from AI, did you look further to find the origin of the information?

Thank you for "digging in" to help all of us.

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Profile picture for Sue, Volunteer Mentor @sueinmn

@helen1000 Good morning Helen, I see you are in research mode today. I really like your second post, where you cite the article then summarize it.

May I ask where you got the information that you used to start the discussion? Can you cite the source? If it came from AI, did you look further to find the origin of the information?

Thank you for "digging in" to help all of us.

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@sueinmn Thanks for your question. For the summary, it is from a FACEBOOK support group about BE. I will try to send the link here. Let me get back to you shortly.

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Unfortunately the authors of this study , who oversaw the study design & coordination , have financial interest in this cell technology . Studies give me hope when they aren’t tied to bias & financial gain .

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https://www.livescience.com/health/medicine-drugs/antibiotic-found-hiding-in-plain-sight-could-treat-dangerous-infections-early-study-finds
A new type of drug, no drug resistance, effective on Gram-positive bacteria, 100 times stronger than original antibiotics.

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https://pubmed.ncbi.nlm.nih.gov/38758004/
Phenotypic amikacin resistance may not indicate poor response to amikacin in Mycobacterium avium complex pulmonary disease

That means, if drug test shows resistant, your body may still have a positive response to the drug. which is a hope to patients.

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Profile picture for helen1000 @helen1000

@sueinmn Here you go-
https://www.facebook.com/groups/469378076532914/
Check the post from Alex Tramp 🙂

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@helen1000 Here is the underlying article from NIH:
https://pmc.ncbi.nlm.nih.gov/articles/PMC11604412/
Here is an excerpt of interest:
"...The study findings are clinically relevant and promising. The autologous transplantation of P63+ lung progenitor cells may restore airway structural integrity in bronchiectasis. Previous studies have revealed that in the lung lesions of people with COPD and cystic fibrosis, stem cells undergo pathological changes that lead to chronic inflammation and unresolved pulmonary damage.9,10 Therefore, targeted therapy at the stem cell level may be essential to the treatment of chronic respiratory diseases, as confirmed by the findings of Yan et al. in bronchiectasis.

While the study has shown promising results, some questions need to be addressed. First, the generalizability of the findings should be further tested in a study with larger sample sizes and multi-center study designs. It would be interesting to determine whether autologous cell transplantation would be equally effective among patients with severe gas exchange dysfunction... A longer follow-up will provide sufficient evidence to evaluate the long-term safety and efficacy, particularly in terms of exacerbation frequency and overall mortality.

Despite the challenges for genetic editing of the stem cells and optimization of the cell sources and delivery methods, cell therapy represents an innovative strategy for chronic respiratory diseases that cannot be reversed by conventional therapy. Fortunately, the preliminary data of the current phase 1/2 trial are promising. Further optimization of the cell transplantation therapy among patients with bronchiectasis needs to be explored in phase 3 clinical trials. Cellular regenerative therapy has now come into reality as a better cure for debilitating airway diseases such as bronchiectasis."

One caution - autologic, cell specific stem cell transplantation - where the patient's own cells must be harvested via bronchoscopy & cell brushing, then grown in a lab before infusion, are EXTREMELY limited and costly at this point. It will be many years before we can walk into a lab at the local hospital and walk out with our own, lab-grown P63+ progenitor cells implanted or infused.

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Profile picture for Sue, Volunteer Mentor @sueinmn

@helen1000 Here is the underlying article from NIH:
https://pmc.ncbi.nlm.nih.gov/articles/PMC11604412/
Here is an excerpt of interest:
"...The study findings are clinically relevant and promising. The autologous transplantation of P63+ lung progenitor cells may restore airway structural integrity in bronchiectasis. Previous studies have revealed that in the lung lesions of people with COPD and cystic fibrosis, stem cells undergo pathological changes that lead to chronic inflammation and unresolved pulmonary damage.9,10 Therefore, targeted therapy at the stem cell level may be essential to the treatment of chronic respiratory diseases, as confirmed by the findings of Yan et al. in bronchiectasis.

While the study has shown promising results, some questions need to be addressed. First, the generalizability of the findings should be further tested in a study with larger sample sizes and multi-center study designs. It would be interesting to determine whether autologous cell transplantation would be equally effective among patients with severe gas exchange dysfunction... A longer follow-up will provide sufficient evidence to evaluate the long-term safety and efficacy, particularly in terms of exacerbation frequency and overall mortality.

Despite the challenges for genetic editing of the stem cells and optimization of the cell sources and delivery methods, cell therapy represents an innovative strategy for chronic respiratory diseases that cannot be reversed by conventional therapy. Fortunately, the preliminary data of the current phase 1/2 trial are promising. Further optimization of the cell transplantation therapy among patients with bronchiectasis needs to be explored in phase 3 clinical trials. Cellular regenerative therapy has now come into reality as a better cure for debilitating airway diseases such as bronchiectasis."

One caution - autologic, cell specific stem cell transplantation - where the patient's own cells must be harvested via bronchoscopy & cell brushing, then grown in a lab before infusion, are EXTREMELY limited and costly at this point. It will be many years before we can walk into a lab at the local hospital and walk out with our own, lab-grown P63+ progenitor cells implanted or infused.

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@sueinmn Yes stem cell therapy is so new and it is not clinically proved yet.

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